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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.
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.
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.
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.