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Micardis (Telmisartan)
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Micardis

Micardis is used to treat high blood pressure (hypertension). This drug works by blocking the hormone angiotensin thereby relaxing blood vessels, causing them to widen. High blood pressure reduction helps prevent strokes, heart attacks, and kidney problems.

Other names for this medication:

Similar Products:
Avapro, Benicar, Cozaar, Diovan, Teveten

 

Also known as:  Telmisartan.

Description

Micardis is a member of a family of drugs called angiotensin receptor blockers (ARBs), which includes losartan (Cozaar), valsartan (Diovan), irbesartan (Avapro), and candesartan (Atacand). ARBs block the ability of the chemical angiotensin II to constrict or squeeze arteries and veins. As a result, the arteries and veins enlarge and blood pressure falls. The reduced pressure in the arteries also makes it easier for the heart to pump blood.

Generic name of Micardis is Telmisartan.

Micardis is also known as Telmisartan, Pritor, Kinzal, Telma, Telday, Teleact D.

Brand name of Micardis is Micardis.

Dosage

Take Micardis orally, usually once a day.

You may take this drug with or without food.

Use Micardis regularly in order to get the most benefit from it.

To help you remember, use Micardis at the same time each day.

For the treatment of high blood pressure, it may take 4 weeks before the full benefit of this drug occurs.

It is important to continue taking this medication even if you feel well.

Most people with high blood pressure do not feel sick.

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

Overdose

If you overdose Micardis and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Tablets should not be removed from the blisters until right before use. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Micardis are:

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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.

Contraindications

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

Be very careful with Micardis if you're pregnant or you plan to have a baby, or you are a nursing mother. This drug can cause serious fetal harm (possibly death) if used during the last six months of pregnancy.

Be careful with Micardis if you have kidney disease, liver disease, high blood levels of potassium, heart problems, severe dehydration (and loss of electrolytes such as sodium), diabetes (poorly controlled), any allergies (especially to ACE inhibitors such as captopril, lisinopril).

To minimize dizziness and lightheadedness, get up slowly when rising from a seated or lying position.

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

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

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

Patients who take medicine for high blood pressure often feel tired or run down for a few weeks after starting treatment.

Elderly patients should be careful with Micardis. They may be more sensitive to its effects.

Avoid alcohol.

Avoid machine driving.

Do not stop taking Micardis suddenly.

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Telmisartan is known to block angiotensin (Ang) II type-1 receptors (AT(1)R), and also activate peroxisome proliferator-activated receptor gamma (PPARgamma) signaling. Recently, PPARgamma has been implicated as a regulator of cellular proliferation and inflammatory responses. In the present study, we investigated the anti-inflammatory effects of telmisartan on middle cerebral artery (MCA) occlusion in mice. Telmisartan was administered orally to mice at 2h before and 2h after MCA occlusion. Infarct size was determined at 24h after MCA occlusion. In addition, cerebral blood flow (CBF) was measured during MCA occlusion. The effect of telmisartan on inflammatory markers, including Iba1 (macrophage/microglia marker) immunoreactivity and plasma high-mobility group box1 (HMGB1), was also investigated at 24h after MCA. Telmisartan significantly decreased the infarct area in dose-dependent manner without affecting CBF. Furthermore, the cerebroprotective effect of telmisartan was inhibited by GW9662, PPARgamma antagonist. Telmisartan significantly decreased the number of Iba1-positive cells expressing HMGB1 and decreased plasma HMGB1 levels. These effects were partially inhibited by GW9662. These data suggest that telmisartan may be a potential treatment for post-ischemic injury by partially inhibiting the inflammatory reaction after cerebral ischemia via a PPARgamma-dependent HMGB1 inhibiting mechanism.

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These findings suggest that telmisartan might contribute to endothelial integrity and vasculogenesis in ischemic regions by increasing numbers of EPCs.

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To examine the association between (healthy) diet, alcohol, protein, and sodium intake, and incidence or progression of CKD among individuals with type 2 diabetes.

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Most hypertensive patients require more than one drug for adequate blood pressure (BP) control. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends starting treatment with a thiazide diuretic or, when BP is >20/10 mm Hg above goal or in patients with diabetes, using two different antihypertensive agents. Searches of Medline, EMBASE, and BIOSIS databases identified four similarly designed, randomized, factorial studies comparing various doses of angiotensin II receptor blockers with hydrochlorothiazide as monotherapy and in combination. The methodology and results of these studies were compared. The primary efficacy end point in these studies was a decrease from baseline in mean diastolic BP after 8 weeks of therapy. All currently available angiotensin I receptor blocker/hydrochlorothiazide combinations evaluated (irbesartan, olmesartan medoxomil, telmisartan, and valsartan plus hydrochlorothiazide) produced significant systolic BP and diastolic BP reductions. Olmesartan medoxomil/hydrochlorothiazide 40 mg/25 mg provided the largest mean reduction in absolute and placebo-corrected systolic BP/diastolic BP. For all angiotensin II receptor blocker/hydrochlorothiazide combinations evaluated, > or =63% of patients achieved a diastolic BP response (diastolic BP <90 mm Hg or > or =10-mm Hg reduction). In conclusion, the combination of an angiotensin II receptor blocker and hydrochlorothiazide produces more substantial BP responses than monotherapy with either component.

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Inflammation is a critical contributing factor to the development and progression of atherosclerosis. Pentraxin 3 (PTX3) is produced abundantly in atherosclerotic lesions while C-reactive protein (CRP) is mainly produced in the liver. In this study, we investigated whether plasma levels of PTX3 might be a sensitive marker both for the severity of coronary artery disease and vulnerable plaques. Next, we determined whether assays for inflammatory molecules can be used to monitor the therapeutic effects of telmisartan on stabilization of vulnerable atherosclerotic plaques.

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The mean age of Chinese patients was 65.6 years, 73.6% of patients were male. The proportion of patients with stroke/transient ischemic attacks at baseline in China was two times more than the entire study population (47.7% vs. 20.9%). In Chinese patients the proportion of permanent discontinuation of study medication due to cough was 0.5% in the telmisartan group, which was much less than that in the combination or the ramipril group. There were no significant differences in the incidence of primary outcome among three treatment groups of Chinese patients. More strokes occurred in Chinese patients than in the entire study population (8.5% vs. 4.5%). Greater systolic blood pressure reduction (-9.8 mmHg), and more renal function failure were noted in the combination treatment group than in the ramipril or telmisartan group (2.6% vs. 1.6% and 1.0%).

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Cardiovascular disease (CVD) accounts for one of every three deaths in the United States. In recent years, a greater understanding of the renin-angiotensin-aldosterone system's (RAAS) contribution to CVD, particularly in the area of blood pressure regulation, has emerged. Thus, interrupting or blocking the RAAS has become a key component in the treatment of hypertension and other cardiovascular conditions. The role of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in reducing CVD in high-risk populations has been demonstrated by two recently completed major trials: the Ongoing Telmisartan Alone and in Combination with Ramipril Global endpoint Trial (ONTARGET) and the Telmisartan Randomized Assessment Study in ACE-Intolerant Subjects with Cardiovascular Disease (TRANSCEND). This article describes these key studies and their outcomes and identifies critical issues that they raise for clinical practice in terms of choosing the most effective therapy for patients with existing CVD.

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Mean 24-hour blood pressure values of ambulatory blood pressure monitoring (ABPM) are more closely related with target organ damage and cardiovascular events in hypertension, than clinic measurements. Both daytime and nighttime blood pressure and short-term blood pressure variability associated with these intermediate and hard cardiovascular outcomes abd should be controlled with antihypertensive treatment. A large increase in blood pressure variability may also occur in the early morning and with some antihypertensive drugs, without a consistent and smooth, more than 24-hour effect. For example, unlike some other angiotensin receptor blockers, telmisartan provides consistent blood pressure reduction for 24-hour, including the critical early morning period.

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Telmisartan, an angiotensin II type 1-receptor blocker (ARBs), has been reported to exert beneficial effects on the central nervous system (CNS). However, the effect of telmisartan on cognitive impairment associated with type 1 diabetes is not well known. Here, we examined the possibility that telmisartan could improve memory function in a type 1 diabetic mouse model, streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice subjected to the Morris Water Maze (MWM) task exhibited a significant decline of spatial learning and memory. Oral administration of telmisartan at two nonhypotensive doses (0.7 or 0.35 mg/kg) significantly improved memory deficits in STZ-induced diabetic mice. Telmisartan treatment markedly reduced Aβ₄₂, APP, BACE1, RAGE, and NF-κB p65 of the hippocampus and cortex, but did not beneficially affect hyperglycemia and hypoinsulinemia in the STZ-induced diabetic mice compared with untreated diabetic mice. Taken together, our findings suggest that telmisartan ameliorates memory deficits in type 1 diabetic mice, at least partly because of attenuation of amyloidosis in the brain.

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It concluded that both Perindopril and Telmisartan significantly reduces systolic, diastolic and mean arterial pressure without any significant effect on renal function in both newly diagnosed and old hypertensive patients.

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20,332 patients (mean age 66 years) were randomised and followed-up for a median of 2.4 years. Recurrent strokes occurred in 916 (9%) patients randomly assigned to ASA with ER-DP and 898 (9%) patients randomly assigned to clopidogrel; 880 (9%) patients randomly assigned to telmisartan and 934 (9%) patients given placebo had recurrent strokes. mRS scores were not statistically different in patients with recurrent stroke who were treated with ASA and ER-DP versus clopidogrel (p=0.38), or with telmisartan versus placebo (p=0.61). There was no significant difference in the proportion of patients with recurrent stroke with a good outcome, as measured with the Barthel index, across all treatment groups. Additionally, there was no significant difference in the median MMSE scores, the percentage of patients with an MMSE score of 24 points or less, the percentage of patients with a drop in MMSE score of 3 points or more between 1 month and the penultimate visit, and the number of patients with dementia among the treatment groups. There were no significant differences in the proportion of patients with cognitive impairment or dementia among the treatment groups.

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Patients with primary hypertension were randomly assigned to perindopril (4 mg/day), Amlodipine (5 mg/day) and telmisartan (80 mg/day) regimen for 3 months (n = 34 each). Brachial-ankle pulse wave velocity (baPWV) was measured by an automatic brachial ankle pulse wave velocity device before the treatment, one-month and three-month after the treatment.

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The authors undertook comparative analysis of the effica,cy and safety of PPARv-activating angiotensin-2 receptor blocker telmisartan (40--80 mg/day) in 80 patients with arterial hypertension (AH) and metabolic disorders (MD). Holter monitoring revealed a more pronounced anti-hypertensive effect of telmisartan compared with enalapril in patients with AH, MD, and compromised renal function. Similarly, telmisartan exerted more apparent positive effect on lipid and carbohydrate metabolism and had renoprotective action in patients with nephrogenic AH (it decreased proteinuria, stabilized creatinine clearance and serum potassium level whereas enalapril caused further deterioration of these parameters). It is concluded that telmisratan is more effective and safer than enalapril in patients with AH and MD.

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Ambulatory BP monitoring demonstrated excellent control rates by telmisartan monotherapy or in combination with hydrochlorothiazide. Observer and measurement bias was substantial based on the changes from baseline by clinical measurements in contrast to ambulatory BP recordings. The successful use of this procedure in primary care research will create further opportunities to define the effectiveness of treatment in the environment in which it is customarily prescribed.

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This study provides insight into the safety of RAS inhibition and Hb correction with an erythrocyte-stimulating agent in kidney transplant recipients.

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Telmisartan increased ACh-induced nitric oxide by 5.5 nmol/l, significantly more than control. Interestingly, cotreatment with GW9662 significantly attenuated telmisartan-induced ACh-induced nitric oxide almost to the levels observed with candesartan. Vascular nitrotyrosine concentration was 1.4 pmol/mg protein in the control group and significantly higher than that in the telmisartan or candesartan group. The lowest nitrotyrosine concentration was observed in the telmisartan group, which was significantly lower than that in the candesartan or telmisartan + GW9662 group. Histology of the thoracic aorta revealed that the plaque area was more significantly decreased in the telmisartan group than in the candesartan or telmisartan + GW9662 group.

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The association between hypertension and an increased risk for Alzheimer's disease (AD) and dementia is well established. Many data suggest that modulation of the renin-angiotensin system may be meaningful for the prevention and therapy of neurodegenerative disorders, in particular AD. Proteolytic cleavage of the amyloid precursor protein (APP) by α-secretase precludes formation of neurotoxic Aβ peptides and is expected to counteract the development of AD. An established approach for the up-regulation of α-secretase cleavage is the activation of G protein-coupled receptors (GPCRs). Therefore, our study aimed to analyze whether stimulation of angiotensin AT1 or AT2 receptors stably expressed in HEK cells influence the nonamyloidogenic pathway of APP processing. Treatment of both receptors with angiotensin II clearly showed that only activation of the AT1 receptor increased several fold the α-secretase-mediated shedding of APP. This effect was completely abolished by treatment with the AT1 receptor-specific antagonist telmisartan. Using the BIM-46187 inhibitor, we demonstrate that the Gαq protein-mediated pathway is involved in this stimulation process. Stimulation of AT1 receptors with the β-arrestin-biased agonist SII was ineffective regarding α-secretase-mediated APP shedding. This result discloses that only the G protein-dependent pathway is involved in the Ang II-induced APP shedding. Blocking of Gβγ subunits by the inhibitor gallein completely prevented constitutive and Ang II-induced APP shedding. Our findings provide evidence that induction of APP shedding via Ang II/AT1 receptor stimulation is effected by G protein activation with Gβγ subunits playing important roles.

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A total of 100 prescriptions were analyzed during the six-month study period. 72% of the patients were in the age group of 65-67 years and this was found to be higher in men 69%. During the study period 80% of the patients were Pre-Hypertensive systolic (80-89 mmHg) and Diastolic (120-139 mmHg) followed by Stage-I Hypertension and Stage-II Hypertension. The most common drug classes involved in the study was Calcium Channel Blockers 37% followed by Angiotensin II receptor antagonists 21% and the most commonly prescribed drugs in the study population were Amlodipine 37%, Losartan 11% and Telmisartan 10%. The most common anti-hypertensive fixed dose combination therapy involved in the study was Telmisartan + Hydrochlorothiazide 15% and most common two drug combination therapy involved in the study was Amlodipine + Atenolol 7% followed by Metoprolol + Amlodipine 1%.

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Animals were divided into 5 groups; a normal control group, an asthma control group, a reference treatment group, receiving dexamethasone, and two treatment groups, receiving telmisartan in two dose levels. Bronchial asthma was induced by intraperitoneal sensitization followed by intranasal challenge with ovalbumin (OVA). Test agents were administered prior to each intranasal OVA challenge. Lung function tests, namely tidal volume (TV) and peak expiratory flow rate (PEF) were assessed 1h after the last challenge. One day after the last challenge, absolute eosinophil counts (AEC) in blood and bronchoalveolar lavage fluids (BALF) were assessed. Serum immunoglobulin E (IgE) as well as BALF total nitrate/nitrite (NOx) were assessed. Oxidative and inflammatory biomarkers, namely lung tissue superoxide dismutase (SOD), glutathione reduced (GSH), tumor necrosis factor-alpha (TNF-α) and interleukin-5 (IL-5), were also assessed, in addition to histopathological study.

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Telmisartan treatment improved insulin sensitivity in obese db/db mice fed a high-fat diet and led to reduction in the size of hypertrophic pancreatic islets in these mice. Moreover, in vitro treatment with telmisartan led to increased expression of Sirt1 mRNA in C2C12 skeletal muscle cells; the increase in Sirt1 mRNA in telmisartan-treated C2C12 myoblasts occurred concomitantly with an increase in AMPK phosphorylation, an increase in NAD+/NADH ratio, and increases in the mRNA levels of PGC1α, FATP1, ACO, and GLUT4.

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micardis online 2016-01-29

Transgenic rats with a brain-specific deficiency in angiotensinogen (TGR(ASrAOGEN)) and the corresponding wild-type, Sprague Dawley (SD) rats were fed (3 months buy micardis ) with a high-calorie cafeteria diet (CD) or standard chow. SD and TGR(ASrAOGEN) rats on the CD diet were also treated with telmisartan (8 mg·kg(-1) ·d(-1) , 3 months).

dosage micardis plus 2015-10-12

Wild-type (WT, C57/B6) and apolipoprotein-E-deficient (ApoE(-/-) ) mice were treated with buy micardis a cholesterol-rich diet for 8 weeks. ApoE(-/-) mice were supplemented with either telmisartan (20 mg·kg(-1) ·day(-1) ), ramipril (2.5 mg·kg(-1) ·day(-1) ) or the combination thereof.

micardis plus generic 2015-10-05

Angiotensin II receptor blockers ( buy micardis ARBs) are widely used to treat hypertension and heart failure. Photosensitivity reactions are cutaneous adverse events due to exposure to a drug and either ultraviolet or visible radiation. Among the ARB class, this type of adverse drug reaction is labeled only for losartan.

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Telmisartan produces a greater reduction in diastolic BP than enalapril and is free from the adverse-effect of dry cough buy micardis that is commonly encountered with enalapril.

micardis 80 mg 2017-07-05

Diabetes was induced by streptozotocin (STZ) (65 mg/kg) in male Wistar rats. One buy micardis diabetic group was treated for 10 weeks with telmisartan (10 mg/kg/day p/o). Pressure-independent aortic pulse wave velocity (PWV) was measured under anaesthesia after intravenous infusion of phenylephrine and nitroglycerine. Aortic wall samples were collected for histomorphometrical analysis.

micardis 8 mg 2017-12-29

Drugs containing buy micardis the carboxylic functional group can be metabolized to form acylglucuronides believed to cause idiosyncratic drug toxicity when the acylglucuronide is unstable. Recent studies have shown that the half-life of an acylglucuronide in phosphate buffer is the best means for classifying acylglucuronides into safe, warning, and withdrawn drugs. However, it is difficult to halt the late stage development of new chemical entities due to the instability of their acylglucuronides. We report an optimized in vitro method for determining the half-lives of acylglucuronides in simple phosphate buffer without the need for authentic standards. The experiment was divided into two incubations. In the first incubation, acylglucuronide was synthesized by human liver microsomes, and in the second incubation, the degradation rate of acylglucuronide in phosphate buffer was determined. The degradation rate constants of acylglucuronides were determined from changes in the LC-MS/MS peak area and the half-lives were calculated. We evaluated the half-lives of 10 drugs: 3 safe drugs (telmisartan, gemfibrozil and flufenamic acid) and 7 withdrawn or warning drugs (zomepirac, diclofenac, furosemide, ibuprofen, S-naproxen, probenecid and tolmetin). The half-lives of the 3 safe drugs were 10.6 h or longer, whereas the half-lives of the 7 withdrawn or warning drugs were 4.0 h or shorter. Although authentic acylglucuronide standards were not used, we obtained half-lives of acylglucuronides in phosphate buffer similar to those reported previously. Using this method, the risk of reactivity caused by acylglucuronides can be evaluated in the early stages of drug discovery.

micardis 160 mg 2017-12-18

The results of this buy micardis pooled analysis of2 PROBE studies in adult patients with mild to moderate essential hypertension suggest that T40/H12.5 and T80/H12.5 conferred greater DBP and SBP control compared with low-dose L50/H12.5, including during the last 6 hours of the dosing interval. All 3 treatments were well tolerated.

co micardis medication 2017-07-02

These findings indicate buy micardis that Ang2, abundantly expressed in neovascularized corneas, has a significant role in inflammation-related driven corneal neovascularization. AT1R may be a therapeutic target for the suppression of corneal neovascularization.

micardis generic 2016-08-27

Prospective observational-study during a mean follow buy micardis -up of 2.1 years.

micardis generic price 2017-08-18

As no or only minor symptoms were observed after ingestion of less than a fivefold MDDw in both children and adults, only symptomatic patients buy micardis and those who have ingested a fivefold MDDw or higher dose should be referred for medical assessment.

micardis hct reviews 2015-04-15

A direct and efficient total synthesis has been developed for telmisartan, a widely prescribed treatment for hypertension. This approach brings together two functionalized benzimidazoles using a high-yielding Suzuki reaction that can be catalyzed by either a homogeneous palladium source or graphene-supported palladium nanoparticles. The ability to perform the cross-coupling buy micardis reaction was facilitated by the regio-controlled preparation of the 2-bromo-1-methylbenzimidazole precursor. This convergent approach provides telmisartan in an overall yield of 72% while circumventing many issues associated with previously reported processes.

micardis hct generic 2017-01-31

Baseline characteristics of each group were similar. During the observation period, the blood pressures of each group decreased at similar rates. In the telmisartan group, 17 patients (47.2%) were introduced to renal replacement therapy, as compared with 31 buy micardis patients (86.1%) in the control group (relative risk 0.55, 95% confidence interval 0.19 - 0.92, p < 0.05). Telmisartan significantly reduced proteinuria levels (from 3.47 +/- 3.00 to 2.41 +/- 2.46 g/g . creatinine, p < 0.05) and was associated with a reduction of 49.6% in the decline rate of eGFR. The incidence of major adverse events in both groups was similar.

dosage micardis hct 2017-11-12

Obesity-related metabolic abnormalities, including chronic inflammation and oxidative stress, increase the risk of colorectal cancer. Dysregulation of the renin-angiotensin system (RAS) also plays a critical role in obesity-related metabolic disorders and in several types of carcinogenesis. In the present study, we examined the effects of an angiotensin-converting enzyme (ACE) inhibitor and angiotensin-II type 1 receptor blocker (ARB), both of which inhibit the RAS, on the development of azoxymethane (AOM)-initiated colonic premalignant lesions in C57BL/KsJ-db/db (db/db) obese mice. Male db/db mice were given 4 weekly subcutaneous injections of AOM (15 mg/kg body weight), and then, they received drinking water containing captopril (ACE inhibitor, 5mg/kg/day) or telmisartan (ARB, 5mg/kg/day) for 7 weeks. At sacrifice, administration of either captopril or telmisartan significantly reduced the total number of colonic premalignant lesions, i.e., aberrant crypt foci and β-catenin accumulated crypts, compared to that observed in the control group. The expression levels of TNF-α mRNA in the colonic mucosa of AOM-treated db/db mice were decreased by captopril and telmisartan. Captopril buy micardis lowered the expression levels of TNF-α, IL-1β, IL-6, and PAI-1 mRNAs, while telmisartan lowered the expression levels of COX-2, IL-1β, IL-6, and PAI-1 mRNAs in the white adipose tissues of these mice. In addition, these agents significantly reduced the levels of urinary 8-OHdG, a surrogate marker of oxidative damage to DNA, in the experimental mice. These findings suggested that both ACE inhibitor and ARB suppress chemically-induced colon carcinogenesis by attenuating chronic inflammation and reducing oxidative stress in obese mice. Therefore, targeting dysregulation of the RAS might be an effective strategy for chemoprevention of colorectal carcinogenesis in obese individuals.

micardis patient reviews 2016-07-18

The immunofluorescent staining showed that administration of vitamin E and telmisartan are attenuated of mononuclear cell infiltration; (p < 0.05 vs. Dox group), also reduced the level of chemokines MCP-1 and ICAM-1 expression compared with Dox group only, and there is marked reduction of myocardial troponin-I levels with improved LV function in vitamin E and telmisartan treated group. Doxorubicin treatment increased MDA, LDH, CK-MB levels significantly (P < 0.01), and were counteracted by administration of vitamin E and telmisartan, but did not significantly buy micardis affect serum catalase activity.

micardis 5 mg 2015-02-18

There was no significant association between renin, aldosterone, the ARR and demographic factors, or BP. Augmentin Tablet Sizes Circadian variations of plasma renin and aldosterone were clearly present. Aldosterone variations were of greater relative amplitude with earlier-occurring peaks than renin. The ARR exhibited statistically and clinically significant circadian variations with the low and peak values averaging 55.9 +/- 32.3 and 161.84 +/- 85.4 pmol/L/ng/dL, respectively. Telmisartan, ramipril, and amlodipine significantly decreased the ARR. Telmisartan had the greatest influence on the ARR. Posture had a clinically significant but statistically nonsignificant effect on the ARR.

micardis drug 2016-10-28

The univariate and multivariate relationships between diabetes status, fasting plasma glucose (FPG), and scores on the Pamelor Generic Complaints Mini-Mental State Examination (MMSE) were assessed.

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The superior LVM regression with telmisartan versus carvedilol suggests telmisartan has a mechanism that may be beyond that Ceftin Antibiotic Dose of lowering BP in hypertensive patients.

micardis brand name 2017-06-26

The study aimed to determine the relationship between left ventricular (LV) diastolic function and the heart's spontaneous baroreflex at rest and in response to orthostatic stress during a prospective follow-up of hypertensive patients with LV hypertrophy (LVH+). LV structure and function and baroreflex sensitivity (BRS) during tilt testing were evaluated in 24 LVH+ patients and compared with 25 age-matched healthy controls and 25 hypertensive patients without LVH (LVH-). Clinical status, Online Buy Nizoral diastolic function and BRS were then assessed in LVH+ patients during treatment with telmisartan (monotherapy or combined with hydrochlorothiazide and/or amlodipine) at 6- and 18-month follow-ups. LVH+ patients had significantly altered diastolic function indices and decreased BRS as compared with healthy controls and LVH- patients. During the 18-month follow-up, favorable changes in diastolic function were associated with improvement in BRS at rest and during tilting. In multivariate regression models, an index reflecting rate of LV myocardial relaxation (E'sept) where E'sept denotes peak early diastolic velocity at the septal mitral annulus and a surrogate for LV filling pressure (E/E'sept), independently from other clinical and echocardiographic variables related to the low-frequency component of BRS during tilting. In conclusion, the LV diastolic function indices have independent associations with BRS parameters obtained at rest and during orthostatic stress in LVH+ patients receiving long-term pharmacological intervention.

micardis medication 2016-06-04

Evidence is currently equivocal on the added benefits of dual blockade of the renin-angiotensin-aldosterone system with the combination of either an ACE inhibitor (ACEI) plus an angiotensin II type 1 receptor antagonist (angiotensin receptor blocker [ARB]) or aliskiren, the first-in-class Requip Max Dosage direct renin inhibitor, plus an ARB.

micardis generic release 2016-10-15

To evaluate Lopid Medicine the facilitating effect of angiotensin II on sympathetic neurotransmission to quantitatively compare the sympatho-inhibitory potencies of the selective AT1 -receptor antagonists losartan, irbesartan and telmisartan in the isolated rabbit thoracic aorta.

micardis 120 mg 2017-09-09

These results suggest that the telmisartan 80 mg/HCTZ 12.5 mg combination provided a more sustained and homogeneous Plavix 90 Mg BP control than nifedipine GITS 60 mg, without producing sympathetic activation.

micardis generic cost 2017-09-27

The pathological hallmark of Rulide Tablets 150mg Alzheimer disease is deposition of amyloid-beta protein (Abeta) in the brain. Telmisartan is a unique angiotensin II receptor blocker with peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-stimulating activity. Activation of PPAR-gamma is expected to prevent inflammation and Abeta accumulation in the brain. We investigated the possible preventive effect of telmisartan on cognitive decline in an Alzheimer disease mouse model via PPAR-gamma activation. Here, male ddY mice underwent ICV injection of Abeta 1-40. Cognitive function was evaluated by the Morris water maze test. A low dose of telmisartan (0.35 mg/kg per day) was administered in drinking water with or without GW9662, a PPAR-gamma antagonist. Cerebral blood flow was evaluated by laser speckle flowmetry. Inflammatory cytokine levels were measured by quantitative RT-PCR. Abeta 1-40 ICV injection significantly impaired cognitive function. Pretreatment with telmisartan improved this cognitive decline to a similar level to that in control mice. Cotreatment with GW9662, a PPAR-gamma antagonist, attenuated this telmisartan-mediated improvement of cognition. Treatment with telmisartan enhanced cerebral blood flow and attenuated the Abeta-induced increase in expression of cytokines, such as tumor necrosis factor-alpha and inducible NO synthase in the brain. Interestingly, coadministration of GW9662 cancelled these beneficial effects of telmisartan. Abeta 1-40 concentration in the brain was significantly decreased by treatment with telmisartan, whereas administration of GW9662 attenuated the decrease in telmisartan-mediated Abeta 1-40 concentration. Taken together, our findings suggest that even a low dose of telmisartan had a preventive effect on cognitive decline in an Alzheimer disease mouse model, partly because of PPAR-gamma activation.

micardis reviews 2015-04-10

The histopathological, stereological, functional and molecular data suggest that telmisartan improves nerve regeneration in peripheral nerve injuries by inhibiting inflammatory cytokine IL-1β and apoptotic caspase-3.

micardis overdose death 2015-05-09

Data from 2 similarly designed prospective, randomized, open-label, blinded-end point (PROBE) studies were pooled and analyzed. The studies were conducted at 72 centers across the United States, and 70 centers in Canada, Europe (9 countries), and the Philippines. Adult male and female patients with mild to moderate essential hypertension (24-hour mean ambulatory diastolic BP [DBP], > or =85 mm Hg; seated cuff DBP, 90-109 mm Hg) were enrolled. Patients were randomly assigned to receive T40/H12.5, L50/H12.5, or T80/H12.5, QD (morning) for 6 weeks. Antihypertensive efficacy was assessed using 24-hour ambulatory BP monitoring (ABPM) and cuff sphygmomanometry at trough, performed at baseline and on completion of active treatment. The primary end point was the reduction from baseline in mean ambulatory DBP over the last 6 hours of the dosing interval. Secondary end points included other ABPM- and clinic-derived changes in DBP and systolic BP (SBP), and control and response rates (SBP response defined as 24-hour mean SBP <130 mm Hg and/or reduction from baseline > or =10 mm Hg; DBP response defined as 24-hour mean DBP <85 mm Hg or reduction from baseline > or =10 mm Hg; DBP control defined as 24-hour mean DBP <85 mm Hg). Tolerability was assessed using patient interview, spontaneous reporting, and clinical evaluation.

micardis 20 mg 2017-10-16

This post hoc analysis does not support dual therapy over monotherapy in high-vascular risk patients with low glomerular filtration rate or albuminuria. This observation is a post hoc comparison and should be interpreted appropriately.