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Micardis (Telmisartan)

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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:
Co-micardis, Deprevex, Domidis, Gliosartan, Kinzal, Kinzalkomb, Kinzalmono, Kinzalplus, Mitosan, Predxal, Pritor, Pritorplus, Saitan, Samertan, Telma, Telmisartanum, Telpres, Telsan, Twynsta

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Avapro, Benicar, Cozaar, Diovan, Teveten

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Also known as:  Telmisartan.


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.


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.


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


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.


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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Fetal and neonatal toxic effects of angiotensin II receptor antagonists have been described in animals and humans. Five cases of fetal or neonatal deaths have been reported following maternal use of sartans for hypertension. We report a case of neonatal transient renal failure following telmisartan therapy during pregnancy. This class of antihypertensive drugs should be avoided during pregnancy and breastfeeding.

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Amlodipine-based antihypertensive combination regimens achieved satisfactory blood pressure control rate in patients with essential hypertension in this patient cohort.

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Patients were divided into 4 groups according to the proportion of in-treatment visits before the occurrence of an event (<25%->75%) in which BP was reduced to <140/90 or <130/80 mm Hg. After adjustment for demographic and clinical variables, a progressive increase in the proportion of visits in which BP was reduced to <140/90 or <130/80 mm Hg was associated with a progressive reduction in the risk of stroke, new onset of microalbuminuria or macroalbuminuria, and return to normoalbuminuria in albuminuric patients. An increased frequency of BP control to either target did not have any consistent effect on the adjusted risk of myocardial infarction and heart failure. The adjusted risk of CV events was reduced by increasing the frequency of BP control to <140/90 mm Hg, but not to <130/80 mm Hg. Similar findings were obtained for the achievement of the BP target in the visit preceding a CV event.

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Blood pressure increases during acute exposure to high altitude in healthy humans. However, little is known on altitude effects in hypertensive subjects or on the treatment efficacy in this condition. Objectives of High Altitude Cardiovascular Research (HIGHCARE)-Andes Lowlanders Study were to investigate the effects of acute high-altitude exposure on 24-hour ambulatory blood pressure in hypertensive subjects and to assess antihypertensive treatment efficacy in this setting. One hundred untreated subjects with mild hypertension (screening blood pressure, 144.1±9.8 mm Hg systolic, 92.0±7.5 mm Hg diastolic) were randomized to double-blind placebo or to telmisartan 80 mg+modified release nifedipine 30 mg combination. Twenty-four-hour ambulatory blood pressure monitoring was performed off-treatment, after 6 weeks of treatment at sea level, on treatment during acute exposure to high altitude (3260 m) and immediately after return to sea level. Eighty-nine patients completed the study (age, 56.4±17.6 years; 52 men/37 women; body mass index, 28.2±3.5 kg/m(2)). Twenty-four-hour systolic blood pressure increased at high altitude in both groups (placebo, 11.0±9 mm Hg; P<0.001 and active treatment, 8.1±10.4 mm Hg; P<0.001). Active treatment reduced 24-hour systolic blood pressure both at sea level and at high altitude (147.9±11.1 versus 132.6±12.4 mm Hg for placebo versus treated; P<0.001; 95% confidence interval of the difference 10.9-19.9 mm Hg) and was well tolerated. Similar results were obtained for diastolic, for daytime blood pressure, and for nighttime blood pressure. Treatment was well tolerated in all conditions. Our study demonstrates that (1) 24-hour blood pressure increases significantly during acute high-altitude exposure in hypertensive subjects and (2) treatment with angiotensin receptor blocker-calcium channel blocker combination is effective and safe in this condition.

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A robust and sensitive high-performance liquid chromatographic-tandem mass spectrometric (HPLC-MS/MS) assay for the high-throughput quantification of the antihypertensive drug azelnidipine in human plasma was developed and validated following bioanalytical validation guidelines. Azelnidipine and internal standard (IS), telmisartan, were extracted from human plasma by precipitation protein and separated on a C18 column using acetonitrile-methanol-ammonium formate with 0.1% formic acid as mobile phase. Detection was performed on a turbo-spray ionization source (ESI) and mass spectrometric positive multiple reaction monitoring mode (+MRM) using the respective transitions m/z 583.3 → 167.2 for azelnidipine and m/z 515.3 → 497.2 for IS. The method has a wide analytical measuring range from 0.0125 to 25 ng/mL. For the lowest limit of quantitation, low, medium and high quality controls, intra- and interassay precisions (relative standard deviation) were 3.30-7.01% and 1.78-8.09%, respectively. The drug was sufficiently stable under all relevant analytical conditions. The main metabolite of azelnidipine, M-1 (aromatized form), was monitored semiquantitatively using the typical transition m/z 581.3 → 167.2. Finally, the method was successfully applied to a clinical pharmacokinetic study in human after a single oral administration of azelnidipine 8 mg. The assay meets criteria for the analysis of samples from large research trials.

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Chronic kidney disease was defined as new microalbuminuria or macroalbuminuria or glomerular filtration rate decline of more than 5% per year at 5.5 years of follow-up. We assessed diet using the modified Alternate Healthy Eating Index (mAHEI). The analyses were adjusted for known risk factors, and competing risk of death was considered.

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There were 20 patients in each group (n=40), with a mean age of 32.65 years in the treatment group. Plasma creatinine did not show any significant change in the different time lapse in which blood samples were taken, but creatinine clearance at the end of surgery (196.415±56.507 vs. 150.1995±75.081; p=0.034), and at 2 h postoperative period (162.105±44.756 vs. 113.235±31.228; p≤0.001) was statistically significant, which supports an increase in renal function in the telmisartan group.

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Induction of diabetes led to a significant increase in retinal production of angiotensin II and AT1R together with ERK activation in the downstream of AT1R. AT1R blockade significantly reversed diabetes-induced electroretinography changes and reduction of synaptophysin protein, but not mRNA, levels in the diabetic retina. In agreement with the AT1R-mediated posttranscriptional downregulation of synaptophysin in vivo, in vitro application of angiotensin II to PC12D neuronal cells caused the UPS-mediated degradation of synaptophysin protein via AT1R, which proved to be induced by ERK activation.

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T, R or T+R had similar beneficial effects on stroke incidence and NO in hypertensive rats, confirming BP reduction as determinant factor in stroke prevention. In contrast, T and T+R provided superior neuroprotection in comparison to R alone in normotensive rats with induced cerebral ischemia.

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AT1R and AT2R expression and cellular localization was demonstrated in MSCs stimulated with VEGF-A and Ang II via quantitative RT-PCR and immunofluorescence, respectively. Differentiation of naïve MSCs in media containing Ang II (2 ng/ml) plus low-dose VEGF-A (2 ng/ml) produced a significantly higher percentage of cells that were positive for expression of EC markers (for example, platelet endothelial cell adhesion molecule, vascular endothelial Cadherin and von Willebrand factor) compared to VEGF-A alone. Ang II alone failed to induce EC marker expression. MSCs differentiated with the combination of Ang II and VEGF-A were capable of forming capillary tubes using an in vitro angiogenesis assay. Induction of EC marker expression was greatly attenuated by co-treatment of Ang II/VEGF-A with the AT2R antagonist PD123319, but not the AT1R antagonist telmisartan.

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To compare the tolerability and safety of telmisartan +/- hydrochlorothiazide (HCTZ).

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To examine drug synergism between angiotensin II AT1-receptor blocker and Ca(2+) channel blocker for lowering blood pressure (BP), telmisartan and lercanidipine were orally injected into to telemetered-spontaneous hypertensive rats and BP was monitored. The highest doses of both drugs (7.66 mg/kg of telmisartan and 1.92 mg/kg of lercanidipine) were clinically relevant at 80 and 20 mg human equivalent doses, respectively, and denoted as dose 1. After constructing the dose-response curve using 0 (vehicle-treated control), 1/16, 1/8, 1/4, 1/2 and 1 doses, all possible combinations of both drugs were tested. Drug synergism in combination therapy of telmisartan with lercanidipine was assessed by calculating the interaction index (γ) as evaluated by γ < 1. We found statistically significant drug synergism in the investigated (telmisartan: lercandipine) combinations of (1/8:1/4), (1/4:1) and (1/8:1). Our results suggest that the combination therapy of telmisartan and lercanidipine at lower doses are effective in lowering BP, and also reduce side effects caused by maximal doses of each drug. Therefore, drug combination of AT1-receptor blocker with Ca(2+) channel blocker is a clinically important tool for the management of hypertension and hypertension-related cardiovascular risks.

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Standardization of the therapeutic inter change process in the hospital setting by the establishment and spreading of standard criteria has been defined as an activity conducent to increased health care quality, and hence improved patient care.

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Baseline characteristics were similar in both groups, including blood pressure, renal function, and proteinuria. Blood pressure control did not differ between groups during follow-up. In the group administered telmisartan, 80 mg once daily, serum creatinine level increased from 1.6 +/- 0.6 to 2.7 +/- 0.9 mg/dL (141 +/- 52 to 239 +/- 80 micromol/L), and estimated creatinine clearance declined from 68 +/- 30 to 50 +/- 34 mL/min (1.13 +/- 0.50 to 0.83 +/- 0.57 mL/s), whereas in those administered 80 mg twice daily, serum creatinine (1.6 +/- 0.7 to 1.6 +/- 0.8 mg/dL [141 +/- 62 to 141 +/- 71 micromol/L]) and estimated creatinine clearance values (67 +/- 38 to 74 +/- 38 mL/min [1.12 +/- 0.63 to 1.23 +/- 0.63 mL/s]) did not change during the study. The decrease in proteinuria was more pronounced (P < 0.01) in patients administered the high dose of telmisartan compared with those treated with the standard dose. Serum potassium levels and lipid profiles did not change significantly in either group.

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Antihypertensive therapy can lower the risk of cardiovascular morbidity and mortality. Yet, partly because of inadequate dosing, wrong pharmacological choices, and poor patient adherence, hypertension control remains suboptimal in the majority of hypertensive patients. Achieving greater blood pressure control requires a multifaceted approach that raises awareness of hypertension, uses effective therapies, and improves adherence. Particular classes of antihypertensive therapy have beneficial actions beyond blood pressure and studies have evaluated differences in cardiovascular protection among classes. The LIFE and HOPE studies showed between-class differences that may be due to effects other than blood pressure-lowering. In the ONTARGET study, telmisartan and ramipril provided similar cardiovascular protection but adherence was higher with telmisartan, which was better tolerated. This difference in compliance is likely to be important for long-term therapy. The selection of an agent for cardiovascular protection should depend on an appreciation of its composite properties, including any beneficial effects on tolerability and increased patient adherence, as these are likely to be advantageous for the long-term management of hypertension. This review examines the evidence that the effects beyond blood pressure provided by some antihypertensive agents can also lower the risk of cardiovascular, cerebrovascular, and renal events in patients with hypertension.

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micardis 80 mg harga 2015-07-30

Induction of diabetes led to a significant increase in retinal production of angiotensin II and AT1R together with ERK activation in the downstream of AT1R. AT1R blockade significantly reversed diabetes-induced electroretinography changes and reduction of synaptophysin protein, but not mRNA, levels in the diabetic retina. In agreement with the AT1R-mediated posttranscriptional downregulation of synaptophysin in vivo, in vitro application of angiotensin II to PC12D neuronal cells caused the UPS-mediated degradation of synaptophysin protein via AT1R, which proved to Motilium 40 Mg be induced by ERK activation.

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The effect of telmisartan Levitra 40 Mg Dosage on ambulatory blood pressure, plasma neurohormonal parameters, and oxidation of serum albumin has not been investigated in hemodialysis (HD) patients. Thirteen hypertensive HD patients were treated with 40 mg telmisartan once daily, and 24-h ambulatory blood pressure monitoring was performed after 0, 4, and 8 weeks of treatment. Plasma renin activity, plasma aldosterone concentration (PAC), brain natriuretic peptide (BNP) level, and serum oxidized albumin level were determined at the same time points. Serum telmisartan concentration was also measured at 4 and 8 weeks. Telmisartan significantly reduced systolic blood pressure and diastolic blood pressure (both awake and sleeping) after 4 weeks, and these pressures showed a further significant decrease after 8 weeks. Plasma levels of aldosterone, BNP, and serum oxidized albumin were markedly decreased after 4 weeks and these lower levels were maintained at 8 weeks. The trough serum telmisartan concentration was not significantly different at 8 weeks compared with 4 weeks. Throughout the treatment period, there were no significant adverse effects. Telmisartan effectively lowers blood pressure and reduces PAC, BNP, and oxidative stress and is safe and well-tolerated by HD patients. A long-term study in a large population is required to determine the influence of telmisartan therapy on cardiovascular mortality and morbidity in HD patients.

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Angiotensin II type 1 receptor (AT1 receptor) blockers (ARBs) are one of the most popular anti-hypertensive agents. Control of blood pressure (BP) by ARBs is now a therapeutic target for the organ protection in patients with hypertension. Recent meta-analysis demonstrated the possibility that telmisartan was the strongest ARB for the reduction of BP in patients with essential hypertension. However, which molecular interactions of telmisartan with the AT1 receptor could explain its strongest BP lowering activity remains unclear. To address the issue, we constructed models for the interaction between commonly used ARBs and AT1 receptor and compared the docking model of telmisartan with that of other ARBs. Telmisartan has a unique binding mode to the AT1 receptor due to its distal benzimidazole portion. This unique portion could explain the highest molecular lipophilicity, the greatest volume distribution and the strongest binding affinity of telmisartan to AT1 receptor. Furthermore, telmisartan was found to firmly bind to the AT1 receptor through the unique "delta lock" structure. Our present study suggests that due to its "delta lock" structure, telmisartan Deltasone Overdose may be superior to other ARBs in halting cardiovascular disease in patients with hypertension.

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Telmisartan, through its antioxidant and Cocaine Viagra Overdose anti-inflammatory actions, effectively prevented cadmium nephrotoxicity in mice. Hence, telmisartan represents a potential candidate to protect the kidney from the detrimental effect of cadmium toxicity.

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The obtained findings suggest that heterocygocity of cytochrome P450 CYP2C9*3 variant in combination with multidrug resistance-associated protein MRP2-24C > T functions as Hyzaar 30 Mg risk factor predisposing to experience drug-drug interaction combing those drugs.

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Risk factors such as hypertension or diabetes result in a continuum of renal damage. Without intervention, initial subclinical endothelial damage progresses to incipient disease, identified by microalbuminuria. Glomerular filtration rate declines, macroalbuminuria develops, and Prednisone Dose Pack Instructions eventually end-stage renal disease (ESRD) emerges. Because of the interrelationship between cardiovascular and renal disease and their common pathophysiologies involving angiotensin II, many patients die of cardiovascular disease before renal replacement therapy is needed. Blood pressure control is key to renoprotection, but blood pressure-independent mechanisms are also implicated. Targeting the renin-angiotensin system (RAS) using angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin receptor blockers (ARBs) is a logical approach to managing all at-risk patients. In advanced nephropathy, therapy aims at retarding progression to ESRD. For incipient nephropathy, ideal therapy should bring about microalbuminuria regression. In patients at risk of renal damage, preventing early target-organ damage is essential. Although evidence of ACE inhibitor benefit is limited, data show that ARBs provide renoprotection throughout the continuum and that this may be related to their cardioprotective effects. More aggressive RAS targeting by combination blockade is under investigation. Telmisartan is an ARB that delays progression of incipient and overt diabetic nephropathy and brings about regression from microalbuminuria to normoalbuminuria in hypertensive and normotensive patients. The ultimate proof of benefit will come from the ONTARGET trial, which will evaluate the cardiovascular and renal protective effects of the combination of telmisartan and ramipril.

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The localization of AT1R and AT2R was shown by immunohistochemistry. EIU was induced by intraperitoneal injection of lipopolysaccharide (LPS). Animals were treated with telmisartan for 2 days and Celexa 10 Mg were evaluated 24 hours later. Expression levels of angiotensin II, STAT3 activation induced by inflammatory cytokines, and retinal proteins essential for neural activities (e.g., synaptophysin, rhodopsin) were analyzed by immunoblot. An AT2R antagonist was administered to evaluate the contribution of AT2R signaling in this therapy. Dark-adapted full-field electroretinography (ERG) was also performed.

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In 2 randomized, double-blind, placebo-controlled trials (total number of patients, 647), telmisartan 40 or 80 mg/d was at least as effective as enalapril 20 mg/d for lowering blood pressure (BP) in patients with mild to moderate hypertension. An open-label, titration-to-response study involving 86 patients with severe hypertension found that telmisartan 80 to 160 mg/d was as efficacious as enalapril 20 to 40 mg/d. The antihypertensive effects of telmisartan 20 to 80 mg/d and enalapril 5 to 20 mg/d were comparable in 278 elderly patients (age > or = 65 years) with mild to moderate hypertension enrolled in a 26-week, double-blind, dose-titration study. A double-blind, titration-to-response study in 71 patients with moderate renal impairment and mild to moderate hypertension found equivalent reductions in Lexapro Higher Than 20 Mg BP with telmisartan 40 to 80 mg/d and enalapril 10 to 20 mg/d without any clinically relevant decline in renal function. Telmisartan tended to be better tolerated than enalapril in this study, with fewer patients experiencing treatment-related adverse events (8.9% vs 26.9%, respectively).

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A total of 100 eligible patients were enrolled in this prospective, open label study. The patients were given telmisartan (40 mg) and chlorthalidone (12.5 mg), who had not achieved the Zofran Zydis Dose target blood pressure (140/90 mmHg) despite taking the combination of telmisartan (40 mg) and hydrochlorothiazide (12.5 mg). The assessment was done at the end of 4 weeks and 8 weeks.

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The potential effects of angiotensin II receptor blockers (ARBs) on adipose tissue biology and body weight are of considerable interest, because these agents are frequently used to treat hypertension in patients who are prone to visceral obesity, the metabolic syndrome, and diabetes. In rats fed a high-fat, high-carbohydrate diet, we compared the effects of 2 ARBs, telmisartan and valsartan, on body weight, food intake, energy expenditure, fat accumulation, fat cell size, and hepatic triglyceride levels. Telmisartan, but not valsartan, promoted increases in caloric expenditure and protected against dietary-induced weight gain. In the telmisartan-treated rats, absolute food intake, but not food intake adjusted for body weight, was lower than in valsartan-treated rats or controls. Telmisartan reduced the accumulation of visceral fat and decreased adipocyte size to a much greater extent than valsartan and was also associated with a significant reduction in hepatic triglyceride levels. Moreover, telmisartan, but not valsartan, increased the expression of both nuclear-encoded and mitochondrial-encoded genes in skeletal muscle known to play important roles in mitochondrial energy metabolism. Thus, in addition to a class effect of ARBs in modulating adipocyte size, these findings raise the possibility that certain molecules, like telmisartan, may have a particularly strong impact on fat cell volume and fat accumulation, as well as distinctive effects on energy metabolism, that may help Combivir Interactions Other Drugs protect against dietary-induced visceral obesity and weight gain.

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Albuminuria, especially macroalbuminuria, and rapid decline of estimated GFR predict hip and pelvic fractures. These findings support a theoretical model of a relationship between underlying causes of microalbuminuria and bone disease.

micardis plus medication side effects 2016-06-20 Identifier: NCT00153062.

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Following haemorrhage mean arterial pressure (MAP) fell by 25-45 mm Hg and was accompanied by a reduction in mesenteric BF without any alteration of mesenteric vascular conductance (VC). While pressor responses to arginine vasopressin remained unaltered, hyporesponsiveness to phenylephrine (10 nmol kg-1) developed 120-180 min after hypotension had been induced. Pressor and mesenteric constrictor responses to angiotensin II (30 pmol kg-1) became significantly blunted as early as 60 min post haemorrhage. The hypotensive effect of an angiotensin1 receptor antagonist, telmisartan (1 mg kg-1), was likewise blunted 3 h after haemorrhage. Pretreatment with the cyclooxygenase inhibitor indomethacin (10 mg kg-1) exaggerated the hypotensive reaction to haemorrhage but did not prevent the development of angiotensin II hyporesponsiveness. In contrast, the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (10 mg kg-1), as investigated 3 h post haemorrhage, restored the systemic pressor responses to angiotensin II and phenylephrine as well as the mesenteric constrictor responses to phenylephrine to normal level and diminished the mesenteric hyporesponsiveness to angiotensin II. Glibenclamide (20 mg kg-1), an inhibitor of ATP-sensitive K- channels given 180 min post haemorrhage, partially reversed haemorrhage-induced hypotension but did not modify angiotensin II hyporesponsiveness.

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Angiotensin Converting Enzyme Inhibitors (ACEI) and Angiotensin Receptor Blockers (ARBs) has been a major therapeutic advance in the management of hypertensive patients. This study was designed to compare adverse effects on renal markers in treatment with two commonly used drugs Perindopril and Telmisartan in cases of Hypertension. This was an 'observational' and 'cross-sectional' study.

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The present study was planned to focus on comparative effects of telmisartan vs lisinopril on blood pressure in patients of metabolic syndrome