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Minipress (Prazosin)

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Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

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Also known as:  Prazosin.


Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.


You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

If you want to achieve most effective results do not stop taking Minipress suddenly.


If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Minipress if you are allergic to Minipress components.

Be careful with Minipress if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

Use Minipress with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

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Previously, we showed that the blockade of α1-adrenoreceptors in the median raphe nucleus (MnR) increased food intake in free-feeding rats, indicating that adrenergic mechanisms in the MnR participate in the regulation of food intake. However, the impact of such a pharmacological manipulation on other neural circuits related to food intake remains unknown. In the current study, we sought to identify forebrain regions which are responsive to α1-adrenergic receptor blockade and presumably involved in the modulation of the feeding response. For this purpose, we examined the induction of c-Fos immunoreactivity in forebrain structures following injections of the α1-adrenoceptor antagonist prazosin into the MnR of free-feeding rats. To determine the chemical identity of hypothalamic c-Fos-positive cells, we then conducted double-label immunohistochemistry for Fos/orexin (OX) or Fos/melanin-concentrating hormone (MCH). Finally, we combined anterograde tracing from the MnR with immunohistochemical detection of orexin. Prazosin injections into the MnR significantly increased food intake. The ingestive response was accompanied by an increase in Fos expression in the basolateral amygdala (BLA) and lateral hypothalamic area (LHA). In the LHA, Fos expression occurred in neurons expressing OX, but not MCH. Combined anterograde tracing experiments revealed that LHA OX neurons are prominently targeted by MnR axons. These findings suggest that intra-MnR injection of prazosin, via activation of orexinergic neurons in the LHA and non-orexinergic neurons in the BLA, evoked a motivational response toward food intake.

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All patients had perspiration and cold extremities. Most of them had sting over extremities except two,having over the trunk. Shock was present in 48(53.3%), whereas myocarditis, encephalopathy, pulmonary edema and priapism were present in 38(42.2%), 32(35.5%), 34(37.8%), and 28(31.1%) children, respectively. Eight (8.9%) children had died. The mean value of blood pressure, sodium and potassium among survivors and non-survivors was insignificant. Mortality was significantly higher in children presented after 6 h of bite. Patients, who had metaboloic acidosis, tachpnea, myocarditis, APE, encephalopathy and priapism had significantly higher mortality (p < 0.05).

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The present study assesses the antinociceptive effect of melatonin in chemical behavioral models of nociception and investigates some of the mechanisms underlying this effect. Melatonin administered by intraperitoneal (i.p., 10-100 mg/kg), intracerebroventricular (i.c.v., 250-500 pmol/site) and intraplantar (, 30-100 ng/ routes, reduced in a dose-dependent manner the nociception caused by injection of glutamate (10 micromol/paw), with mean ID50 values of 32.6 mg/kg, 200 pmol/site and 59 ng/, respectively. Furthermore, melatonin in the dose range of 10-100 mg/kg, i.p., reduced the neurogenic pain caused by injection of capsaicin (5.2 nmol/paw) with inhibition of 48 +/- 4%. The antinociceptive effect of melatonin (100 mg/kg, i.p.) on glutamate-induced nociception was completely prevented by the pretreatment of animals with naloxone (a nonselective opioid receptor antagonist, 1 mg/kg, i.p.), ketanserin (a preferential 5-HT2A receptor antagonist, 1 mg/kg, i.p.), sulpiride (a D2 receptor antagonist, 50 mg/kg, i.p.), L-arginine (a precursor of nitric oxide, 600 mg/kg, i.p.), yohimbine (an alpha2-adrenoceptor antagonist, 0.15 mg/kg, i.p.) and luzindole (a preferential MT2 receptor antagonist, 10 mg/kg, i.p.), but was not affected by the pretreatment with D-arginine (an inactive isomer of L-arginine, 600 mg/kg, i.p.), prazosin (an alpha1-adrenoceptor antagonist, 0.15 mg/kg, i.p.) or after bilateral adrenalectomy. Collectively, present results suggest that melatonin produces peripheral and central antinociception when assessed on capsaicin- or glutamate-induced pain in mice through mechanisms that are likely mediated by interaction with plasma membrane-bound melatonin receptors and modulated by opioid, serotonergic (5-HT2A receptors), dopaminergic (D2-receptors), adrenergic (alpha2-adrenoceptors) systems as well as the L-arginine-nitric oxide pathway.

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Spontaneous isometric contractions and field-evoked responses were recorded in vitro from strips of bovine mesenteric lymph node capsule. Field stimulation (0.3 ms pulses, 60 V nominal, 2 min trains) at frequencies > or = 2 Hz evoked a frequency-dependent increase in baseline tension which was maximum at frequencies > or = 16 Hz. Evoked contractions were significantly reduced (P = 0.02) by the neurotoxin tetrodotoxin (10(-6) M) although they were unaffected by the alpha-adrenoceptor antagonists phentolamine, rauwolscine and prazosin (3 x 10(-6) M). Similarly, responses were unaffected by the beta-adrenoceptor antagonist propranolol (10(-6) M), the cholinergic antagonist atropine (10(-6) M) or the uptake blocker cocaine (10(-6) M). Field-evoked contraction was also unaffected by a 30 min exposure to alpha,beta-methylene ATP (10(-6) M). The results suggest that bovine lymph node capsular smooth muscle is innervated by excitatory nerves which are non-adrenergic, non-cholinergic and non-purinergic in nature.

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An LC-MS method for the determination of metoclopramide in human plasma was developed and validated. Sample preparation involved extraction with ethyl acetate. Chromatographic separation was performed on a Thermo Hypersil-Hypurity C18 (150 mm x 2.1 mm, 5 microm) with the mobile phase consisting of 40 mM ammonium acetate-methanol-acetonitrile. A single-quadrupole mass spectrometer with an electrospray interface was operated in the selected-ion monitoring mode to detect the [M+H]+ ions at m/z 300 for metoclopramide and at m/z 384 for the internal standard (prazosin). The method was validated over 0.78-50.00 ng mL(-1) for metoclopramide. The recovery was 67.8-83.1%, and the limit of quantitation (LOQ) detection was 0.78 ng mL(-1) for metoclopramide. The intra- and inter-day precision of the method at three concentrations was 5.0-13.6% with accuracy of 99.2-104.0%. Stability of compounds was established in a battery of stability studies. The method was successfully applied to bioequivalence studies of metoclopramide hydrochloride tablets to obtain the pharmacokinetic parameters.

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Intravenously injected lipopolysaccharides (LPS) rapidly induce pulmonary platelet accumulation (PPA) and anaphylaxis-like shock (ALS) in mice. Macrophages reportedly release catecholamines rapidly upon stimulation with LPS. Here, we examined the involvement of macrophage-derived catecholamines in LPS-induced PPA and ALS. A catecholamine or Klebsiella O3 (KO3) LPS was intravenously injected into mice, with 5-hydroxytryptamine in the lung being measured as a platelet marker. The tested catecholamines induced PPA, leading to shock. Their minimum shock-inducing doses were at the nmol/kg level. The effects of epinephrine and norepinephrine were inhibited by prazosin (α1 antagonist) and by yohimbine (α2 antagonist), while dopamine's were inhibited only by prazosin. Use of synthetic adrenergic α1- and/or α2-agonists, platelet- or macrophage-depleted mice, a complement C5 inhibitor and C5-deficient mice revealed that (a) α2-receptor-mediated PPA and shock depend on both macrophages and complements, while α1-receptor-mediated PPA and shock depend on neither macrophages nor complements, (b) the PPA and ALS induced by KO3-LPS depend on α1- and α2-receptors, macrophages, and complements, and (c) KO3-LPS-induced PPA is preceded by catecholamines decreasing in serum. Together, these results suggest the following. (i) Catecholamines may stimulate macrophages and release complement C5 via α2-receptors. (ii) Macrophage-derived catecholamines may mediate LPS-induced PPA and ALS. (iii) Moderate PPA may serve as a defense mechanism to remove excess catecholamines from the circulation by promoting their rapid uptake, thus preventing excessive systemic effects. (iv) The present findings might provide an insight into possible future pharmacological strategies against such diseases as shock and acute respiratory distress syndrome.

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The dorsal motor nucleus of the vagus (DMV) receives more noradrenergic terminals than any other medullary nucleus; few studies, however, have examined the effects of norepinephrine (NE) on DMV neurons. Using whole cell recordings in thin slices, we determined the effects of NE on identified gastric-projecting DMV neurons. Twenty-five percent of DMV neurons were unresponsive to NE, whereas the remaining 75% responded to NE with either an excitation (49%), an inhibition (26%), or an inhibition followed by an excitation (4%). Antrum/pylorus- and corpus-projecting neurons responded to NE with a similar percentage of excitatory (49 and 59%, respectively) and inhibitory (20% for both groups) responses. A lower percentage of excitatory (37%) and a higher percentage of inhibitory (36%) responses were, however, observed in fundus-projecting neurons. In all groups, pretreatment with prazosin or phenylephrine antagonized or mimicked the NE-induced excitation, respectively. Pretreatment with yohimbine or UK-14304 antagonized or mimicked the NE-induced inhibition, respectively. These data suggest that NE depolarization is mediated by alpha(1)-adrenoceptors, whereas NE hyperpolarization is mediated by alpha(2)-adrenoceptors. In 16 neurons depolarized by NE, amplitude of the action potential afterhyperpolarization (AHP) and its kinetics of decay (tau) were significantly reduced vs. control. No differences were found on the amplitude and tau of AHP in neurons hyperpolarized by NE. Using immunohistochemical techniques, we found that the distribution of tyrosine hydroxylase fibers within the DMV was significantly different within the mediolateral extent of DMV; however, distribution of cells responding to NE did not show a specific pattern of localization.

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The antagonistic effect (pA2) of prazosin for norepinephrine was 7.76+/-0.13 in young dogs and 7.62+/-0.06 in aged dogs. The specific binding of [3H]-tamsulosin (a relatively selective alpha1A-adrenoceptor antagonist) was recognized diffusely in proximal urethras with in vitro autoradiography. The density of binding in smooth muscles was approximately 60 and 40% in circular longitudinal layers, respectively, for both dogs.

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Posterior reversible encephalopathy syndrome (PRES) is a condition characterized by varying degrees of headache, nausea, vomiting, visual disturbances, focal neurologic deficit, and seizures due to severe systemic hypertension. The knowledge of secondary hypertension in children is most commonly due to renal abnormalities, suggesting that the leading cause of PRES in childhood is renal diseases.

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Strips of canine saphenous vein, inferior vena cava, and femoral artery were studied isometrically in vitro to compare quantitatively the alpha 1- and postsynaptic alpha 2-adrenoceptor contributions to the contractile force generated by l-norepinephrine (NE). Effects mediated by each receptor type were measured independently by quantitative blockade of virtually all alpha 1-receptors with prazosin, or alpha 2-receptors with rauwolscine. Appropriate concentrations of the antagonists were calculated from dissociation constants previously determined by binding or competition with [3H]prazosin or [3H]rauwolscine in tissue homogenates. The contribution of alpha 1-adrenoceptors was larger than that of alpha 2-receptors in all vessels. The alpha 2-type was responsible for 38% of the maximum unblocked response to NE in saphenous vein, 32% in vena cava, and 28% in femoral artery. The occupation-response relationship for alpha 1-receptors was almost linear, without the marked upward convexity reported in some other vessels. alpha 2-Occupation-response curves were convex towards the occupation axis, with a relatively small response at low levels of occupation.

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The proportion of patients who reported treatment-emergent dizziness was not significantly different between the 2 treatment groups (tadalafil 7.0%; placebo 5.7%; P = .403). No difference between treatment groups was observed with respect to patients meeting the criteria for a positive orthostatic test (30 per treatment group, P = 1.00). The incidence of discontinuations was low among both treatment groups.

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This study evaluated the effect of prazosin in controlled mild hypertension and evaluated select metabolic changes that occurred with prazosin monotherapy. Various aspects of glucose, insulin, and lipid metabolism were studied before and after approximately 10 weeks of prazosin treatment in 12 patients with mild hypertension. Prazosin was well tolerated and induced a significant decrease (p less than 0.001) in both systolic and diastolic blood pressures, without any change in body weight. Plasma concentrations of glucose, free fatty acid, and lactate, which were measured hourly from 8 A.M. to 4 P.M. following meals consumed at 8 A.M. and noon, did not change with prazosin treatment. However, the plasma insulin response from 8 A.M. to 4 P.M. decreased significantly (p less than 0.001) following prazosin treatment. In addition, fasting plasma triglyceride and cholesterol concentrations were significantly lower (p less than 0.05) in prazosin-treated persons, as were postprandial triglyceride concentrations (p less than 0.001). Lower total plasma triglyceride and cholesterol concentrations were accounted for by decreases in very low-density lipoprotein cholesterol and triglyceride and low-density lipoprotein cholesterol and triglyceride, whereas both high-density lipoprotein triglyceride and high-density lipoprotein cholesterol concentrations increased following prazosin treatment. Finally, although both apolipoprotein A1 and apolipoprotein B concentrations decreased in association with prazosin treatment, the decrease in apolipoprotein B was much greater in magnitude, leading to an increase in the ratio of apolipoprotein A1 to apolipoprotein B. In this study, treatment of mild hypertension with prazosin led to lower blood pressures and changes in insulin and lipoprotein metabolism that are important in this patient population.

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The role of alpha-1 and alpha-2 adrenoceptors in the contractile response of the proximal urethra to agonists and antagonists was studies in female and male New Zealand White rabbits. The response pattern for alpha-1 agonists showed a sharp rise, while that for alpha-2 agonists showed a gradual increase to a maximum pressure. The duration of the response of alpha-2 agonists was significantly longer than that of alpha-1 agonists. A difference in the response between alpha-1 and alpha-2 would be produced mainly through different receptor functions. The magnitude of the response of alpha-1 adrenoceptors in the male rabbits was almost twice that of the female rabbits. In contrast, the response of alpha-2 in the male rabbits was less than that of the female rabbits. Our experimental findings indicate that alpha-2 stimulation mediates a slow and prolonged response that is essential for urinary continence in female rabbits.

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1. We examined whether alpha 1-adrenoceptors in various blood vessels can be divided into subtypes by antagonist affinity or by susceptibility to chloroethylclonidine or nifedipine. 2. Noradrenaline or phenylephrine produced concentration-dependent contractions in all the tissues tested, which were competitively inhibited by phentolamine, yohimbine, prazosin, WB4101 and HV723. However, there were large differences between the tissues in the pA2 values for all the antagonists except phentolamine. 3. The blood vessels could be classified into three groups (I, II and III) on the basis of their affinity variation. In group I (dog mesenteric artery and vein, saphenous vein), the pA2 values for HV723 were greater than 9, and those for HV723 and WB4101 were approximately 1 log unit higher than for prazosin. This rank order of affinity reversed in group II (dog carotid artery and rat thoracic aorta), where prazosin was more potent (pA2 values greater than 9.5) than HV723 or WB4101. In group III (rabbit mesenteric artery, thoracic aorta and carotid artery and guinea-pig thoracic aorta), on the other hand, prazosin, HV723 and WB4101 inhibited the noradrenaline response with a similar affinity (pA2 values ranging from 8 to 9). 4. Yohimbine inhibited the responses to noradrenaline and phenylephrine with a lower affinity than prazosin, HV723 or WB4101. The pA2 values for yohimbine were similar in groups I and II (the values greater than 6.5), which were greater than those in group III (values less than 6.4). 5. The alpha l-adrenoceptors in group II were selectively affected by chlorethylclonidine, resulting in an irreversible attenuation of noradrenaline responses in the dog carotid artery and a persistent contraction in the rat thoracic aorta. 6. Nifedipine either produced no effect or a slight inhibition of alpha l-adrenoceptor-mediated contractions in all the blood vessels; these effects were not correlated to the above groups. 7. These results suggest that alpha,-adrenoceptors of blood vessels can be divided into three subtypes (designated as alpha 1H, alpha4L and alpha 1N) by antagonist affinity and their susceptibility to chloroethylclonidine but not to nifedipine: the characteristics of each subtype are summarized in Table 3. Subtypes alpha lH, alpha 1L and alpha lN may be predominantly involved in the contractile responses to noradrenaline or phenylephrine of the blood vessels in groups II, III and I, respectively.

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La présente étude visait à examiner et comparer les effets antagonistes de l’atipamezole, la yohimbine et le prazosin sur la diurèse induite par la xylazine chez des chats cliniquement normaux. Cinq chats furent utilisés de manière répétée dans chacun des neuf groupes. Un groupe n’était pas médicamenté. Les chats dans les autres groupes reçurent de la xylazine par voie intramusculaire à un dosage de 2 mg/kg de poids corporel (PC), et de la saline (comme témoin); 160 μg/kg PC de prazosin; ou 40, 160, ou 480 μg/kg PC d’atipamezole ou de yohimbine par voie intraveineuse 0,5 h plus tard. Des échantillons d’urine et de sang furent prélevés 10 fois sur une période de 8 h. On mesura le volume, le pH, et la gravité spécifique de l’urine; la concentration plasmatique d’arginine vasopressine (AVP); les valeurs de créatinine, d’osmolalité, et d’électrolytes dans l’urine et le plasma ont également été mesurées. Autant l’atipamezole que la yohimbine ont antagonisé la diurèse induite par la xylazine, mais pas le prazosin. L’effet antidiurétique de l’atipamezole était plus puissant que celui de la yohimbine mais n’était pas dose-dépendant, contrairement à l’effet de la yohimbine aux doses testées. Autant l’atipamezole que la yohimbine ont renversé les diminutions induites par la xylazine de la gravité spécifique et l’osmolalité de l’urine, et l’augmentation de la clairance de l’eau libre. Le taux de filtration glomérulaire, la clairance osmolaire, et les concentrations d’électrolytes plasmatiques n’étaient pas affectés de manière significative. L’antidiurèse de l’atipamezole ou la yohimbine n’était pas liée à la surface sous la courbe de la concentration d’AVP, bien que les doses les plus élevées d’atipamezole et de yohimbine augmentèrent initialement et de manière temporaire la concentration d’AVP plasmatique, suggérant ainsi que ceci pourrait influencer partiellement les effets antidiurétiques de ces deux agents. L’effet diurétique de la xylazine chez les chats peut être médié par des adrénorécepteurs-α2 mais pas par des adrénorécepteurs-α1. L’atipamezole et la yohimbine peuvent être utilisés comme agents antagonistes contre la diurèse induite par la xylazine chez des chats cliniquement normaux.(Traduit par Docteur Serge Messier).

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Drinking mate or chimarrão, a hot infusion of Ilex paraguariensis (ILEX) leaves, is a common habit in Southern South America that has a social and almost ritualistic role. It has been used as a stimulant beverage in South America and analgesic in regions of Argentina for treatment of headache and others painful inflammatory conditions such as arthritis and rheumatism.

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The combination of alpha-blockade and calcium antagonism has not previously been studied and should be useful for resistant hypertensives who have not tolerated beta-blockade or ACE inhibitors. The combination of ACE inhibition and calcium antagonism has previously been shown to be additive; its use as a positive control in the present studies suggests that the use of an active drug for a run-in period may be a useful design for permitting the study of patients from whom all treatment cannot safely be withdrawn.

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1. The interaction between chloroethylclonidine (CEC) and noradrenaline (NA) has been examined at alpha-adrenoceptors mediating contractions of rat aorta. 2. In rat aorta, the competitive antagonist prazosin, over the concentration-range 0.01-10 microM, produced concentration-dependent shifts in the contractile potency of NA, so that there was no component of the NA contraction resistant to prazosin. 3. The irreversible alpha 1-adrenoceptor antagonists, phenoxybenzamine (PBZ) (1-10 microM) and benextramine (10 microM) produced shifts in potency of NA and reduced the maximum response in a concentration-dependent manner. 4. The irreversible alpha 1-adrenoceptor antagonist, CEC (100 microM), produced a non-parallel shift in the NA concentration-response curve so that low concentrations of NA produced relatively small contractions but relatively high concentrations produced further contractions, so that the maximum response was not significantly reduced. 5. The combination of CEC pretreatment and subsequent prazosin (0.1 microM) produced a parallel shift in the potency of NA. However, prazosin (10 microM) failed to produce any further effect on the response to high concentrations of NA following CEC pretreatment. Hence, a component of the contraction to NA in the presence of CEC was resistant to subsequent prazosin. Likewise, this component was resistant to a combination of prazosin (10 microM) and yohimbine (10 microM). 6. Receptor protection experiments were carried out in which tissues were exposed to NA (100 microM), yohimbine (10 microM) or prazosin (0.1 microM) prior to and during exposure to CEC. Receptor protection with NA, yohimbine or prazosin (0.1 microM), followed by washout prevented the shift in potency of NA produced by CEC. 7. Further experiments examined the effects of prazosin (10 microM) on responses to NA following receptor protection with NA (100 microM), yohimbine (10 microM), prazosin (10 microM), or xylazine (100 microM). In receptor protection studies with NA, subsequent prazosin (10 microM) produced a shift in response to NA following CEC which was not signficantly different from the shift produced by prazosin alone in the absence of receptor protection. In receptor protection studies with prazosin, yohimbine or xylazine, subsequent prazosin (10 microM) produced shifts in the response to NA following CEC which were significantly less than the shift produced by prazosin alone in the absence of receptor protection.8. It is concluded that CEC has two actions in the rat aorta. Firstly, it behaves as an irreversible a,-adrenoceptor antagonist, reducing the response to low concentrations of NA (up to 10 microM). However,after exposure to CEC, concentrations of NA of 10 microM and above produced contractions resistant toprazosin. This resistant component was still present following receptor protection with alpha1,- or alpha2-adrenoceptor antagonists, but absent following receptor protection with NA. Hence, the latter response may represent an irreversible agonist interaction between CEC, NA and alpha-adrenoceptors which cannot be affected by subsequent competitive antagonism, but which can be prevented by receptor protection with the agonist NA prior to CEC.

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The peripheral mechanisms responsible for pressor response produced by microinjections of baclofen (GABA(B) agonist) into the nucleus tractus solitarii (NTS) of conscious rats were studied. Bilateral microinjections of baclofen (10-1,000 pmol/100 nl) produced a dose-related increase in mean arterial pressure (MAP) and heart rate. The maximal response was observed after 15 min. Intravenous injection of prazosin decreased MAP to control levels. Subsequent treatment with Manning compound (vasopressin receptor antagonist; iv) produced an additional decrease in MAP. In a different group of rats, vasopressin antagonist was injected first and MAP was significantly decreased; however, it remained elevated compared with prebaclofen injection levels. Subsequent treatment with prazosin abolished the baclofen-induced pressor response. Reductions in baclofen-induced pressor response with prazosin treatment were followed by a reflex tachycardia in animals that received a 100 pmol/100 nl dose of baclofen. The tachycardia was not observed with a dose of 1,000 pmol/100 nl. The pressor response induced by microinjection of baclofen into the NTS of conscious rats may be produced by both increases in sympathetic tonus and vasopressin release.

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The [3H]-verapamil binding activity of rat cardiac sarcolemmal fragments was studied, using membranes harvested from non-perfused, aerobically-perfused and ischaemic hearts. Glass-fibre filters were found to contain specific, high affinity--(KD 38 +/- 3.1 nM) [3H]-verapamil binding sites--making them unsuitable for use in [3H]-verapamil binding studies. Incubation of membranes from non-perfused hearts in a medium containing 150 mM NaCl, 1 mM CaCl2 and 50 mM Tris revealed two populations of [3H]-verapamil binding sites. When centrifugation instead of filtration was used to separate bound and free [3H]-verapamil, high affinity sites with a KD of 0.57 +/- 0.19 microM and a Bmax of 38 +/- 5.2 pmol mg-1 protein, and low affinity sites with a KD of 78 +/- 27.5 microM and a Bmax of 2.9 +/- 1.3 nmol mg-1 protein were detected. However, only low affinity binding sites could be detected in membranes which had been incubated in a cation-free medium containing 50 mM Tris. [3H]-verapamil binding to the low and high affinity sites was saturable, reversible, stereospecific and displaceable by D600 greater than diltiazem greater than Ca2+ but not by nifedipine, nitrendipine, nisoldipine or prazosin. The two populations of binding sites survived aerobic perfusion and 60 min ischaemia at 37 degrees C. Ischaemia reduced the Bmax and KD but selectivity was maintained.

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Hypertension is an underlying risk factor for cardiovascular disease. Despite this, its pathogenesis remains unknown in most cases. Recently, the transient receptor potential (TRP) channel family was associated with the development of several cardiovascular diseases linked to hypertension. The melastatin TRP channels TRPM4 and TRPM5 have distinct properties within the TRP channel family: they form nonselective cation channels activated by intracellular calcium ions. Here we report the identification of TRPM4 proteins in endothelial cells, heart, kidney, and chromaffin cells from the adrenal gland, suggesting that they have a role in the cardiovascular system. Consistent with this hypothesis, Trpm4 gene deletion in mice altered long-term regulation of blood pressure toward hypertensive levels. No changes in locomotor activity, renin-angiotensin system function, electrolyte and fluid balance, vascular contractility, and cardiac contractility under basal conditions were observed. By contrast, inhibition of ganglionic transmission with either hexamethonium or prazosin abolished the difference in blood pressure between Trpm4-/- and wild-type mice. Strikingly, plasma epinephrine concentration as well as urinary excretion of catecholamine metabolites were substantially elevated in Trpm4-/- mice. In freshly isolated chromaffin cells, lack of TRPM4 was shown to cause markedly more acetylcholine-induced exocytotic release events, while neither cytosolic calcium concentration, size, nor density of vesicles were different. We therefore conclude that TRPM4 proteins limit catecholamine release from chromaffin cells and that this contributes to increased sympathetic tone and hypertension.

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Placebo administration did not affect any hemodynamic values. Terlipressin administration, on the other hand, resulted in expected changes on the hepatic venous pressure gradient, hepatic blood flow, and systemic hemodynamics. In contrast, prazosin significantly decreased hepatic venous pressure gradient with an increased hepatic blood flow and intrinsic hepatic clearance. After terlipressin administration, a further decrease in hepatic venous pressure gradient was observed with preservation of hepatic blood flow and intrinsic hepatic clearance. The magnitude of decrease in hepatic venous pressure gradient was more profound in patients receiving prazosin plus terlipressin than in those receiving terlipressin alone. However, the magnitude of changes in systemic hemodynamics was no different between the two groups of patients.

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Medical treatment of distal ureteral stones with doxazosin has similar stone passage rate, expulsion time, and safety in women compared with men.

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In this in vitro study on the human umbilical artery, the effects of N(omega)-nitro-L-arginine methyl ester (L-NAME), indomethacin, prazosin, yohimbine and propranolol on the responses induced by bupivacaine and ropivacaine were investigated. Arteries isolated from umbilical cords from women who did not exhibit systemic diseases, who were not on medication and who had normal full-term deliveries, were cut into spiral strips 12 x 3 mm. Strips were mounted in organ baths at 37 degrees C continuously gassed with 5% CO(2) in oxygen. The responses to the drugs were recorded isometrically on a polygraph. In the bupivacaine study, when we administered cumulative concentrations of bupivacaine (10(-9) - 10(-4) M; n = 6) on basal tonus, there was no relaxation or contraction response on the tissue. Strips were precontracted with serotonin (10(-6)M 5-HT) then bupivacaine (10(-9) - 10(-4) M) was directly administered cumulatively. In the ropivacaine group, when cumulative concentrations of ropivacaine (10(-9) - 10(-4) M; n = 6) were administered on the tissue, preconstricted with 5-HT, ropivacaine did not alter the contraction response. Ropivacaine (10(-9) - 10(-4) M) was directly administered to the bath. Though bupivacaine produced relaxation, ropivacaine produced contraction (P < 0.05). Indomethacin, prazosin, yohimbine and propranolol did not significantly alter these responses. In addition, it was demonstrated that L-NAME did not affect the relaxation responses induced by bupivacaine. Thus adrenergic receptors, nitric oxide syntenaze and prostaglandins do not appear to affect the responses induced by these two local anesthetics.

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The purposes of this study were to investigate the level of the sympathetic nervous system in which nitric oxide (NO) mediates regional sympathetic vasoconstriction and to determine whether neural mechanisms are involved in vasoconstriction after NO inhibition. Ganglionic blockade (hexamethonium), alpha1-receptor blockade (prazosin), and spinal section at T1 were used to study sympathetic involvement. NO was blocked with Nomega-nitro-L-arginine methyl ester (L-NAME). Regional blood flow in the mesenteric and renal arteries and terminal aorta was monitored by electromagnetic flowmetry in conscious rats. L-NAME (3-5 mg/kg iv) increased arterial pressure and peripheral resistance. Ganglionic blockade (25 mg/kg iv) significantly reduced the increase in resistance in the mesentery and kidney in intact and spinal-sectioned rats. Ganglionic blockade significantly decreased hindquarter resistance in intact rats but not in spinal-sectioned rats. Prazosin (200 micrograms/kg iv) significantly reduced the increased hindquarter resistance. We concluded that NO suppresses sympathetic vasoconstriction in the mesentery and kidney at the spinal level, whereas hindquarter tone is mediated at supraspinal and synaptic levels.

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In this study, the mechanism of action of dexfenfluramine (DEXF) at the hepatic level was investigated. The drug is shown to bind to the alpha 1-adrenergic receptor and to increase intracellular calcium in isolated rat hepatocytes, thereby activating phosphorylase via a calcium-dependent mechanism. Moreover, phosphorylase activation by DEXF was inhibited by different agents that interfere with the alpha 1-adrenergic signalling system: prazosin, phorbol 12 alpha-myristate 13 beta-acetate (PMA), and DEXF itself. We also show that phosphorylase activation induced by catecholamines and analogues (epinephrine, phenylephrine), whose actions are mediated by a calcium-dependent mechanism, was counteracted by the drug in the submillimolar range (0.1-1 mM). The activation of glycogenolysis by the drug is accompanied by a stimulation of the glycolytic flux (54% increase in lactate plus pyruvate accumulation), consistent with an increase in fructose-2,6-bisphosphate (F-2,6-BP) levels (36%). These results indicate that the interaction of DEXF with the alpha 1-adrenergic receptor channels glucose 6-phosphate derived from glycogen away from glucose production into the glycolytic pathway.

minipress medicine

1. We have characterized alpha 1-adrenoceptor in the conduction systems of the rat heart by quantitative autoradiography. 2. Consecutive 20 micron thick sections from a single rat heart containing the sinoatrial (SA) node and atrioventricular (AV) node were incubated with increasing concentrations of [3H]-prazosin with or without 10 microM phentolamine. After exposure to 3H-Ultrofilm, optical densities corresponding to the SA node and AV node were determined by computerized densitometry after comparison with 3H standards. 3. The SA node and AV node were stained heavily for cholinesterase and they contained a higher concentration of alpha 1-adrenoceptors than the adjacent myocardium without a significant change in the affinity. 4. These results support the hypothesis that alpha 1-adrenoceptors may play an important role not only in inotropism but also in chronotropism of rat hearts.

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minipress 2 mg 2017-01-03

1. Crude venom gland extracts (VGE) were prepared from female Delena cancerides and Isopeda montana spiders. The VGE were tested in isolated rat atrial, caudal artery and pithed rat preparations for pharmacological activity. 2. In rat isolated atrial preparations, D. cancerides and I. montana VGE, each in a concentration of 2 glands/mL, produced increases in atrial rate which were abolished by propranolol (1 mumol/L) but not by ketanserin (0.1 mumol/L) or reserpine pretreatment (2.5 mg/kg s.c. 24 h prior to experimentation) indicating a direct action on atrial beta-adrenoceptors. 3. In rat caudal artery preparations each VGE buy minipress produced an increase in perfusion pressure, which was taken as an index of vasoconstriction. Pressor responses to D. cancerides VGE (1 gland/mL) were abolished in the presence of prazosin (1 mol/L) but not by reserpine pretreatment, indicating an action of the VGE on vascular alpha 1-adrenoceptors. Neither prazosin nor reserpine pretreatment had any effect on pressor responses of rat caudal artery preparations to I. montana VGE. Ketanserin (6 nmol/L) produced a small reduction in the degree of vasoconstriction produced by the VGE. This demonstrates a lack of alpha 1-adrenoceptor agonist activity of the VGE. 4. Both VGE produced dose-dependent increases in mean arterial pressure and heart rate in pithed rat preparations. The use of relatively selective receptor antagonists indicated that the increases in mean arterial pressure (MAP) produced by both VGE were mediated by an action on alpha 2-adrenoceptors.

minipress tablets 2016-01-08

1. In freely moving rats, intestinal blood flow, aortic blood pressure and blood pressure at the base of mesenteric arcades were measured simultaneously so as to determine the role of feed arteries and of the microcirculation in the control of intestinal vascular resistance. Segmental resistances of feed arteries (Rfeed) and of microcirculatory vessels (Rmicro) were calculated. 2. At rest, Rfeed and Rmicro were 32 and 68%, respectively, of the total intestinal vascular resistance. 3. Injection of noradrenaline (2 micrograms i.v,) increased Rfeed by 151% and Rmicro by 243%. Angiotensin II (400 ng i.v.) did not increase Rfeed significantly, but increased Rmicro by 239%. Conversely, serotonin (15 micrograms i.v.) increased Rfeed by 414% but did not affect Rmicro significantly. 4. Spontaneous physical activity increased Rfeed by 29% and Rmicro by 39%, while sudden environmental stress increased Rfeed by 116% and Rmicro by 129%. Infused noradrenaline (1 microgram min-1 i.v.) or adrenaline (0.8 microgram min-1 i.v.) reduced intestinal flow by 21 and 16% respectively, while noradrenaline, but not adrenaline, increased intestinal resistances. 5. alpha 1-Blockade with prazosin (0.1 mg i.v.) reduced Rfeed and Rmicro by 43 and 16%, buy minipress respectively. Thereafter, environmental stress decreased Rfeed by 24% while Rmicro was unaffected. Intravenous noradrenaline and adrenaline responses were attenuated. 6. We conclude that in freely moving rats, mesenteric feed arteries, as well as microcirculatory vessels, are true resistance vessels, and that both participate in the control of intestinal blood flow.

minipress medication information 2015-05-15

AT1 antagonists should be avoided throughout pregnancy. If these agents are prescribed accidentally to a pregnant woman, monitoring of amniotic fluid volume and beta2-microglobulin buy minipress fetal blood levels after discontinuation of the AT1 antagonist can provide critical data for advising parents on pregnancy and fetal outcome.

minipress xl drug 2015-12-19

Biliary excretion of thyroxine (T4),3,5,3'-triiodothyronine (T3),3,3,5'-triiodothyronine (rT3) and diiodothyronines (3,3'-T2,3,5-T2 and 3',5'-T2) was estimated with the aid of radioimmunoassay in 3-4 subsequent 2-h samples of bile obtained from pentobarbital anesthetized rats through the tubing inserted in bile duct. The excretion of T3 was significantly decreased during 4-h infusion of 2400 ng/kg/min adrenaline in normal rats or during 6-h infusion of the latter dose in the animals preinjected with 2 micrograms T4. Moreover, the excretion of buy minipress rT3 was significantly increased after the infusion of 1200 and 2400 ng/kg/min adrenaline. Such increase after 1200 and 2400 ng/kg/min adrenaline was prevented by a single dose of 10 mg/kg phentolamine (alpha 1-2-antagonist) and that after 2400 ng/kg/min adrenaline also by 2.5 mg/kg prazosin (alpha 1-antagonist) injected at the beginning of the infusion, but not by 6 mg/kg yohimbine (alpha 2-antagonist) injected every 60 min during 4-h infusion. In addition, increased rT3 excretion was found during the infusion of alpha 1-agonist methoxamine (1.5 mg/kg/4 h), while no such effect of the infusion of alpha 2-agonist azepexol (10 mg/kg/4 h) was observed. It may be suggested that the effect of adrenaline was mediated predominantly by alpha 1-adrenoceptors and that the observed changes in biliary excretion of T3 and rT3 were related to the inhibition of 5'-monodeiodination in the liver.

minipress pill 2015-07-26

The ability of noradrenaline (NA) to stimulate increases in high-affinity GTPase activity in sarcolemma-enriched rat aorta and caudal artery membranes was examined in the present study. In aortic membranes, NA significantly (P < 0.05; N = 5) increased the Vmax from a basal value of 103 +/- 29 to 156 +/- 38 pmol Pi/min/mg protein, but did not affect the Km which was 0.32 +/- 0.08 microM in the absence and 0.58 +/- 0.16 microM in the presence of NA. However, in caudal artery membranes, NA significantly (P < 0.05; N = 6) increased both the Vmax and the Km from basal values of 69 +/- 12 pmol Pi/min/mg protein and 0.24 +/- 0.05 microM, respectively, to 205 +/- 54 pmol Pi/min/mg protein and 1.01 +/- 0.25 microM, respectively. Removing the endothelium from both artery preparations did not alter significantly basal GTPase activity or the magnitude of the increase stimulated by NA. Prazosin significantly inhibited NA-stimulated increases in GTPase activity in membranes from endothelium-denuded caudal artery and aorta, and in endothelium-intact caudal buy minipress artery membranes. However, yohimbine significantly inhibited NA-stimulated increases in GTPase activity only in preparations from endothelium-intact caudal arteries. Therefore, in endothelium-intact caudal artery membranes, NA stimulated increases in GTPase activity that were apparently mediated by both alpha 1-adrenoceptors and alpha 2-adrenoceptors, while in endothelium-denuded aortic and caudal artery membranes this increase was mediated solely by alpha 1-adrenoceptors. Western blotting of these arteries confirmed the presence of both Gi alpha 2,3 and Gq/11 alpha, which are candidates for mediating the alpha 1-adrenoceptor-stimulated increases in GTPase activity.

minipress 1mg capsule 2017-02-21

Nociceptive stimulation induces pulmonary vasoconstriction in fetuses and newborns. The mechanism of this response buy minipress is not fully understood. As the systemic hemodynamic response to pain is mainly mediated by sympathetic stimulation, we hypothesized that pain-induced pulmonary vasoconstriction results from the activation of catecholaminergic receptors. To test this hypothesis, we studied the pulmonary vascular response to nociceptive stimuli in fetal lambs before and after alpha-adrenoceptor blockade.

minipress drug information 2016-11-23

N(G)-(Nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide synthase, induces catalepsy in mice. The objective of the present work was to investigate if buy minipress serotonergic drugs are able to modulate this effect. Results showed that the cataleptogenic effect of L-NOARG (40 mg/kg) in male albino-Swiss mice was enhanced by pre-treatment with (+)-N-tert-butyl-3-(4-[2-methoxyphenyl]piperazin-1-yl)-2-phenylpro panamide ((+)-WAY-100135, 5 or 10 mg/kg), a 5-HT1A-selective receptor antagonist, and by ketanserin (5 or 10 mg/kg), a 5-HT2A receptor and alpha1-adrenoceptor antagonist. Prazosin (3 or 5 mg/kg), an alpha1-adrenoceptor antagonist, and endo-N-(8-methyl-8-azabicyclo[3.2.1]oct-3yl)-2,3-dihydro-3,3-dimet hyl-indole-1-carboxamide HCl (BRL-46470A, 0.05 or 0.5 mg/kg), a 5-HT3 receptor antagonist, did not interfere with L-NOARG-induced catalepsy. Ritanserin (3 or 10 mg/kg), a 5-HT2A and 5-HT2C receptor antagonist, tended to enhance the effect of L-NOARG. These results confirm that interference with the formation of nitric oxide induces catalepsy in mice, and suggest that this effect is modulated by 5-HT1A and 5-HT2A receptors.

minipress tablets dose 2017-07-12

Depolarization can alter the expression of membrane receptors and change certain receptor-mediated events, but previous studies have not assessed the impact of depolarization on generation of arachidonic acid and its metabolites (AA) in nonexcitable tissues. We assessed AA generation in Madin-Darby canine kidney (MDCK) cells grown for 3 days buy minipress in increased extracellular [K+], which is known to acutely depolarize these cells. Growth under these conditions resulted in decreases in the number of alpha 1-adrenergic receptors (alpha 1 AR), a small decrease in receptor-mediated phosphoinositide hydrolysis, but increases in alpha 1 AR-mediated prostaglandin E2 formation and AA release. Calcium ionophore (A23187)-, melittin-, and bradykinin-stimulated AA release were also enhanced. The reduction in alpha 1 AR number and increased AA release were substantially reduced or eliminated when K(+)-treated cells were grown in the absence of extracellular calcium. The results provide evidence that hormone-stimulated AA release and prostaglandin production can be enhanced by chronic exposure to elevated extracellular K+ concentration, perhaps as a consequence of a depolarization-induced enhancement in phospholipase A2 activity. The results provide evidence for the parallel and independent regulation of the pathways for receptor-mediated phosphoinositide hydrolysis (phospholipase C activation) and AA release (phospholipase A2 activation) in MDCK cells.

minipress xl tablets 2015-08-12

Terazosin and its enantiomers, antagonists of alpha 1-adrenoceptors, were studied in radioligand binding and functional assays to determine relative potencies at subtypes of alpha 1- and alpha 2-adrenoceptors in vitro. The racemic compound and its enantiomers showed high and apparently equal affinity for subtypes of alpha 1-adrenoceptors with Kl values in the low nanomolar range, and showed potent antagonism of alpha 1-adrenoceptors in isolated tissues, with buy minipress the enantiomers approximately equipotent to the racemate at each alpha 1-adrenoceptor subtype. At alpha 2b sites, R(+) terazosin bound less potently than either the S(-) enantiomer or racemate. R(+) terazosin was also less potent than the S(-) enantiomer or the racemate at rat atrial alpha 2B receptors. These agents were not significantly different in their potencies at alpha 2a or alpha 2A sites. Since the high affinity for alpha 2B sites of quinazoline-type alpha-adrenoceptor antagonists has been used to differentiate alpha 2-adrenoceptor subtypes, the low affinity of R(+) terazosin for these sites was unexpected. Because terazosin or its enantiomers are approximately equipotent at alpha 1-adrenoceptor subtypes, the lower potency of R(+) terazosin at alpha 2B receptors indicates a somewhat greater selectivity for alpha 1-compared to alpha 2B adrenoceptor subtypes. The possible pharmacological significance of this observation is discussed.

minipress xl dose 2015-10-28

Chronic nonbacterial prostatitis/chronic pelvic pain syndrome is unsatisfactorily defined and insufficiently studied illness. Also, the treatment success is questionable and therefore, this illness is a therapeutical problem for urologists--which medications are the best choice in treating this uncomfortable condition? This paper presents results of prospective, open, analytical, comparative study that was performed on 90 patients with diagnosed chronic nonbacterial prostatitis/chronic pelvic pain syndrome. Patients were divided into three groups and were treated with two medications ciprofloxacin (C), doxazosin (D) and combination of ciprofloxacin + doxazosin (C+D). The effects were measured using symptom questionnaire for prostate illnesses of the National Institute for Health - USA (NIH-CPSI). During the basic evaluation, sum ranging from 0 buy minipress to 43 was calculated for each patient. This number is called total sum NIH-CPSI (National Institutes of Health Chronic Prostatitis Symptom Index) of the questionnaire, which generates the questions from 1 to 9. The most significant change occurred in C+D group where the total sum changed from 18-38 in the beginning to 5-31 at the end of the treatment (55,1% (p<0,001)). Significant changes were also found in D group where the change was 46, 4% (p<0,001). At the end of the treatment no significant change was registered in C group (p<0,005): p<0,001--significance threshold. Combination of ciprofloxacin + doxazosin proved to be the best choice for treatment.

minipress overdose symptoms 2017-03-06

Changes in alpha1-adrenoceptor (alpha1AR) gene expression in the rat liver during different phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Septic rats exhibit two metabolically distinct phases: an initial hyperglycemic phase (9 h after CLP, early sepsis) followed by a hypoglycemic phase (18 h after CLP; late sepsis). The [3H]prazosin binding studies show that the density of alpha1AR was increased by 30% during the early phase while it was decreased by 24% during the late phase of sepsis. Western blot analyses reveal that alpha1AR protein level was elevated by 48% during early sepsis but was decreased by 55% during late sepsis. Northern blot analyses depict that the steady-state level of alpha1bAR mRNA was enhanced by 21% during the early phase but was declined by 29% during the late phase of sepsis. Nuclear run-off assays show that the transcription rate of alpha1bAR gene transcript was increased by 76% during early buy minipress sepsis while it was decreased by 29% during late sepsis. The actinomycin D pulse-chase studies indicate that the half-life of alpha1bAR mRNA remained unaffected during the early and the late phases of sepsis. These findings demonstrate that during the early phase of sepsis, the increase in the rate of transcription of alpha1bAR gene paralleled with the elevations in the alpha1bAR mRNA abundance and alpha1AR protein level, while during the late phase of sepsis, the decrease in the rate of transcription of alpha1bAR gene coincided with the declines in the alpha1bAR mRNA abundance and the alpha1AR protein level in the rat liver. These observations indicate that the altered expression of alpha1AR genes in the rat liver during the progression of sepsis was regulated transcriptionally.

minipress drug class 2016-11-29

The effects of dopexamine hydrochloride on sympathetic neuroeffector transmission were studied in rabbit isolated pulmonary artery. Short-term buy minipress exposure of dopexamine (10(-8) x 10(-7) M) and cocaine (10(-6)-3 x 10(-5) M), but not desipramine (3 x 10(-9)-3 x 10(-7) M), to the artery enhanced the contractions evoked by electrical-field stimulation. Corticosterone (4 x 10(-5) M), corticosterone (4 x 10(-5) M) plus cocaine (3 x 10(-8) M), but not cocaine (3 x 10(-5) M), attenuated the enhancement seen with dopexamine. High concentrations of dopexamine (10(-5)-3 x 10(-5) M), cocaine (10(-4) M), and desipramine (10(-6)-10(-5) M) decreased the stimulation-evoked contractions. Dopexamine (10(-7)-3 x 10(-5) M), but neither cocaine nor desipramine, caused an increase in resting tension that waned with time. Corticosterone (4 x 10(-5) M), but not cocaine (3 x 10(-5) M), attenuated the increase in resting tension. Propranolol (10(-6) M) did not alter the enhancing and inhibitory effects of dopexamine. A single concentration (10(-7) and 10(-6) M) of either dopexamine or desipramine caused a time-dependent biphasic response as regards the repetitive stimulation-evoked contractions of pulmonary artery: initial enhancement followed by inhibition. The inhibitory effect of dopexamine (10(-6) M) and desipramine (3 x 10(-6) M) seen after prolonged exposure was almost irreversible and partially reversible, respectively, by washing the preparations with drug-free salt solution. Cocaine caused a monophasic steady-state response: either enhancement (10(-5) M) or inhibition (2 x 10(-4) M). In both cases, the onset was rapid. The reduction caused by cocaine (2 x 10(-4) M) and by prazosin (10(-9) M) was fully reversed. Dopexamine (10(-5) M) antagonized competitively the contractions evoked by noradrenaline (3 x 10(-9)-10(-4) M). It is concluded that (1) the dopexamine-induced enhancement of neurogenic contractions is not due to either inhibition of neuronal and extraneuronal uptake of noradrenaline or an agonist action on prejunctional beta 2-adrenoceptors; (2) that the dopexamine-induced inhibition of stimulation-evoked contraction is due to an inhibition of postjunctional alpha 1-adrenoceptors; and (3) that the dopexamine-induced increase in resting tension is due to its metabolite methyldopexamine.

minipress drug 2015-04-25

Retrospective Lexapro 10 Mg case-control study.

minipress ptsd dosage 2015-06-16

In hypertensive patients, elevated serum cholesterol is a frequent and sinister additional coronary risk factor. Selective alpha 1-adrenoreceptor inhibitors appear to have the unique ability to control both risk factors. Forty-two patients, ages 42 to 65 years, including 21 men with sustained hypertension and elevated serum cholesterol levels, were included in a trial of monotherapy with doxazosin administered once daily (range, 1 to 16 mg). The influence of the drug on high blood pressure and elevated serum cholesterol was evaluated over a 28-week period, which consisted of a 4-week, single-blind placebo lead-in period, an open 10-week dose-adjustment period, and finally a 14-week maintenance period. Of the 39 efficacy-evaluable patients, 25 (64%) achieved adequate blood pressure control (diastolic blood pressure less than 90 mm Reglan Ppi Medication Hg or a decrease in diastolic blood pressure greater than 10 mm Hg) at a mean daily dose of 2 mg of doxazosin. No persistent changes occurred in heart rate. In the 32 patients with evaluable lipid data, there were nonsignificant trends to an increase in high-density lipoprotein cholesterol and a reduction in total cholesterol, together with a significant reduction in serum triglyceride concentration. The combined changes in blood pressure and blood lipid levels resulted in a reduction of 36% in the calculated risk of coronary heart disease. Eleven patients reported side effects and four were withdrawn from therapy. These results confirm the antihypertensive and anticholesterolemic efficacy of once-daily treatment with doxazosin.(ABSTRACT TRUNCATED AT 250 WORDS)

minipress reviews 2015-04-28

Isolated rat tail artery rings model was employed to evaluate the vasodilative effects of drugs, mice tail thrombosis model induced by carrageenan was used to study the antithrombotic effects Anafranil With Alcohol and its molecular mechanisms of the drug composition.

minipress capsules 2015-04-03

Nightmares are a common feature of posttraumatic stress disorder Buspar Xl Dosage (PTSD) and are frequently resistant to treatment. Two emerging treatments for nightmares are pharmacotherapy with prazosin and psychotherapy using imagery rehearsal (IR). A case illustration demonstrates the application of these treatments with a client suffering from chronic, severe PTSD. The case illustrates the use of these strategies for managing PTSD-related nightmares, as well as the novel approach of scheduled awakenings following relapse.

minipress and alcohol 2015-04-12

The effect of a newly synthesized irreversible blocker of the alpha-1 receptor [1-(4-amino-6,7-dimethoxy-2-quinazolnyl)-4-(2-bicyclo[2,2,2] octa-2,5-dienylcarbonyl)-piperazine; SZL-49] has been evaluated in contractile studies in rabbit aorta and binding studies in aorta and brain. SZL-49 produced long lasting inhibition of norepinephrine-induced contractions which was apparent 21 hr after drug washout. The inhibition, which was dose and time dependent, was characterized by progressive shift to the right in the norepinephrine dose-response curve. The ED50 for norepinephrine was shifted from 10(-7) M to 8 X 10(-7), 3 X 10(-6), 1 X 10(-5) and 5 X 10(-4) M after incubation (30 min) and washout of increasing concentrations of SZL-49. Surprisingly, SZL-49, irrespective of the dose or incubation time, did not decrease the maximal response of aortic rings to norepinephrine. This resulted in a norepinephrine dose-response curve after SZL-treatment that is parallel to the control. SZL-49 had no effect on the spasmogenic actions of histamine, serotonin, KCl or CaCl2. In contrast to the inhibitory pattern seen with SZL-49, incubation with 10(-7) M phenoxybenzamine shifted the norepinephrine dose-response curve to the right in a nonparallel manner and significantly depressed the maximal response obtainable with norepinephrine. Incubation with 10(-6) M phenoxybenzamine for 30 min virtually abolished the response to norepinephrine. Phenoxybenzamine (10(-7) M) was without effect on aortic rings treated with a maximally effective dose of SZL-49. Prazosin weakly antagonized the contractile actions of norepinephrine observed after SZL-49 treatment, whereas yohimbine was without effect on these norepinephrine-induced contractions. In control binding studies [3H]prazosin bound to two classes of sites in both aorta and brain preparations. Affinities and densities for these sites were K1 = 67.5 pM, K2 = 309 pM; R1 = 38.2 fmol/mg, R2 = 46.47 fmol/mg in aorta and K1 = 29.6 pM, K2 = 182 pM; R1 = 6.6 fmol/mg and R2 = 30.4 fmol/mg in brain. Treatment with increasing amounts of SZL-49 (10(-10) to 10(-8) M) progressively reduced the number of [3H]prazosin sites without altering the affinity of the sites remaining. At 10(-7) M, SZL-49 eliminated completely all specific [3H]prazosin binding. Our results indicate that the site mediating norepinephrine contraction after treatment with SZL-49 does not possess the characteristics of an alpha-1 receptor and supports the hypothesis Sinemet Cr Generic that a low affinity site for norepinephrine and prazosin exists in vascular smooth muscle.(ABSTRACT TRUNCATED AT 400 WORDS)

minipress overdose death 2016-02-17

The effects of hypothyroidism on whole body thermogenesis, brown adipose tissue recruitment state, and alpha 1-adrenergic receptor density were investigated. Treatment of rats with methimazole for 4-5 wk led, as expected, to reduction of growth and resting metabolic rate. The thermogenic response to norepinephrine injection was practically abolished. Generally, only small effects of hypothyroidism on brown adipose tissue were observed: total protein content, mitochondrial GDP binding capacity, and total content of the uncoupling protein thermogenin were not altered. The density of beta-adrenergic receptors (estimated with [3H]CGP-12177 as a ligand) was also unchanged. However, the density of alpha 1-adrenergic receptors (estimated with [3H Aricept Drug Class ]prazosin) was markedly increased; in other physiological conditions, such an increase has been associated with an increased degree of recruitment of the tissue. These data indicate that brown adipose tissue in the subthermoneutral hypothyroid animal, probably due to homeostatic mechanisms, is exposed to an increased sympathetic stimulation, leading to an increased alpha 1-adrenoceptor density. However, other features of recruitment are only poorly induced, probably due to attenuation of the beta-adrenergic signaling mechanism. The increased alpha 1-adrenergic receptor density may be responsible for certain altered features of brown adipose tissue in hypothyroid animals, such as peroxisomal recruitment and perhaps also for maintenance of the thermogenin content. The results also indicate that the increased alpha 1-adrenergic density generally seen in recruitment would not result from chronic beta-adrenergic stimulation of the tissue but may be controlled via another regulatory pathway, e.g., via the alpha 1-adrenergic pathway itself.

minipress generic name 2016-10-13

Deep skin burns are characterised by progressive ischemia secondary to vasoconstriction and thrombosis formation. Burn trauma elicits increased sympathetic activity and elevation of circulating catecholamines acting on adrenoceptors in vascular tissue playing an important role in the regulation of organ blood flow. The present study in rats investigated the role of alpha- and beta-adrenoceptors in the circulatory changes taking place in normal skin and in partial- and full-thickness skin burns using laser Doppler flowmetry. Evaluation was based on intravenous administration Coreg 5 Mg of the following adrenergic agonists and antagonists: l-phenylephrine (alpha(1)-agonist), prazosin (alpha(1)-antagonist), clonidine (alpha(2)-agonist), yohimbine (alpha(2)-antagonist), prenalterol (beta(1)-agonist), terbutaline (beta(2)-agonist), and propranolol (beta(1)- and beta(2)-antagonist). Blood flow in normal skin was reduced by phenylephrine (p<0.001), clonidine (p<0.001) and propranolol (p<0.01), and increased by prazosin (p<0.05), yohimbine (p<0.05), prenalterol (p<0.05) and terbutaline (p<0.01). In partial-thickness burns, blood flow was reduced by phenylephrine (p<0.01), clonidine (p<0.01) and propranolol (p<0.05). In full-thickness burns, only clonidine reduced perfusion (p<0.05). In conclusion, beta(1)- and beta(2)-adrenoceptors play important role in the physiological regulation of skin perfusion but are of lesser importance for postburn skin perfusion. Vasoconstrictive alpha(1)- and alpha(2)-adrenoceptors were shown to be tonically active in normal skin and in partial-thickness burns, exerting a negative effect on skin perfusion which was further potentiated by exogenous administration of alpha(1)- and alpha(2)-agonists and reversed by selective alpha-blockers. In full-thickness burns, activation of alpha(2)-receptors was shown to significantly impair skin circulation, raising a flag of warning for the use of clonidine to treat pain in burn patients.

minipress cost 2016-07-26

Excitatory junction potentials (e.j.p.s) evoked by nerve stimulation with 15 pulses at 1 Hz were recorded from muscle cells of the rabbit isolated mesenteric artery. Clonidine and B-HT 933 depressed all e.j.p.s in the train. The percentage inhibition was inversely related to the number of pulses. Yohimbine, rauwolscine and tolazoline reduced the early e.j.p. amplitudes but enhanced the later ones. The percentage facilitation of e.j.p.s increased with the number of pulses until Suprax Suspension Price a maximum was reached. Prazosin and corynanthine did not influence the first few e.j.p.s but potentiated the subsequent ones; their effects were less pronounced than those of yohimbine and rauwolscine. All the drugs antagonized the inhibition by clonidine but the effects of yohimbine and rauwolscine were more marked than those of prazosin and corynanthine. Phenylephrine, St 587 and noradrenaline depressed the e.j.p.s. Yohimbine diminished the effects of these substances and was a stronger antagonist of phenylephrine than prazosin. We suggest that, in the rabbit mesenteric artery, noradrenaline and the neuroeffector transmitter (probably ATP) are co-released from the terminals of postganglionic sympathetic nerves. Noradrenaline activates presynaptic alpha 2-adrenoceptors and thereby depresses transmitter release. The degree of presynaptic inhibition depends on the number of pulses applied, i.e. on the biophase concentration of noradrenaline.

minipress tab 2015-09-13

Aggressive behavior was significantly correlated with alpha1-adrenoceptor number in patients with AD ( Mobic Reviews R(s)=0.454, N=24). Furthermore, patients receiving ongoing neuroleptics had significantly higher Bmax for [3H] prazosin (21 +/- 2, N=9) than those who were not (16 +/- 1, N=15).

minipress overdose 2015-11-29

To investigate functional aspects of sympathetic nerve influence on the urethral rhabdosphincter, we examined electrical potentials of the male feline rhabdosphincter evoked by hypogastric nerve (HGN) stimulation using electromyography. Hypogastric nerve stimulation (1 Hz) elicited electrical potentials of the rhabdosphincter in both normal and chronically rhizotomized cats. In normal cats, the evoked potentials were not affected by transection of the bilateral pudendal nerves. The amplitudes of the evoked potentials were significantly larger in rhizotomized cats (p < 0.001), while the threshold stimuli and latency periods were not. These evoked potentials were prazosin- and atropine-resistant, but were abolished by hexamethonium and pancuronium in both groups. In normal cats, high frequency stimulation (10 to 20 Hz) of the HGN increased the Sustiva Renal Dosing activity of the rhabdosphincter when the bladder was empty, but not when the bladder was full enough to trigger the vesicourethral relaxation reflex. This excitatory effect of HGN stimulation was blocked by prazosin. These data suggest that the potential of the rhabdosphincter evoked by HGN stimulation (1 Hz) is produced through synapse from sympathetic preganglionic to cholinergic postganglionic neurons, and that, after sacral rhizotomy, cholinergic postganglionic terminals form more effective functional connections to somatically denervated motor end-plates of the rhabdosphincter. The sympathetic nerve is also believed to play a role in modulating urethral afferent activities through action on urethral smooth muscle.

minipress drug interactions 2016-11-05

Prazosin has been reported to reduce the hypotensive and/or bradycardic effect of clonidine in various animal models. Investigations in humans have given conflicting conclusions about the effectiveness of the combination of clonidine and prazosin. In patients with essential hypertension prazosin significantly reduced Biaxin With Alcohol the hypotensive effect of intravenous clonidine, but it failed to affect the clonidine-induced bradycardia. This finding means that the combination of prazosin and clonidine is inappropriate in antihypertensive therapy.