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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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this study was a randomized, multicenter, double-blind, parallel group, Phase III, 8-week clinical trial to compare the superiority of the S-AM/TEL 2.5/40-mg and S-AM/TEL 5/40-mg combinations with TEL 80-mg mono-therapy. The primary end point was the change in the mean sitting diastolic blood pressure from baseline (week 0) after 8 weeks of therapy between treatment groups.

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In a prospective double-blind study, patients with hypertension and coronary artery disease were treated with either 40 mg telmisartan (n = 21) or placebo (n = 21) for 12 weeks. General markers of inflammation, such as high-sensitivity C-reactive protein (hs-CRP) and interleukin-6 (IL-6), and cell adhesion molecules, such as soluble intercellular adhesion molecule (s-ICAM-1) and the leucocyte adhesion molecule soluble-L-selectin (sL-selectin), as well as the lymphocytic expression of the beta2 integrin MAC-1, were assessed before and after treatment. Telmisartan therapy significantly decreased the lymphocyte beta2 integrin MAC-1 expression, whereas hs-CRP, IL-6, s-ICAM and sL-selectin remained unaltered. In-vitro experiments were conducted to clarify the mode of action. Cultured human lymphocytes were stimulated with either angiotensin II or phorbol-12-myristate-13-acetate (PMA)/ionomycin, alone or after pretreatment with telmisartan. Whereas angiotensin II exerted no effect on beta2-integrin MAC-1 expression in lymphocytes, telmisartan dose-dependently inhibited beta2-integrin expression in lymphocytes in the absence or presence of angiotensin II.

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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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We examined the effects of telmisartan on cholesterol transport-related proteins (apolipoprotein E [ApoE]/low-density lipoprotein receptor [LDL-R]) and microtubule-associated protein 2 (MAP2) in the brain of spontaneously hypertensive stroke resistant (SHR-SR). SHR-SR received transient middle cerebral artery occlusion (tMCAO) for 90 minutes at 12 weeks of age and then was divided into 3 experiment groups including a vehicle, low-dose telmisartan (.3 mg/kg/day), and high-dose telmisartan (3 mg/kg/day).

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Insulin resistance predicts development of type 2 diabetes mellitus (DM). Adipocytes release tumor Necrosis factor-alpha (TNF-α), and adiponectin. They modulate whole-body insulin sensitivity . The disturbance in the relationship between good and bad adipokines may cause insulin resistance. The renin-angiotensin aldosteron system (RAAS) plays a role in DM and the consequence of cardiovascular complications development. It is considered as a target for therapy. The present objective examined the relationship between renin angiotensin system and DM. There were, Group (1): Normal non obese rats, Group (2): Obese diabetic rats, Group (3): Obese diabetic rats with telmisartan, Group (4): Obese diabetic rats with enalapril, Group (5): Obese diabetic rats with aliskiren. There was a significant increase in serum glucose, lipid profile [triglycerides (TGs), low-density lipoprotein cholesterol (LDL), total serum cholesterol (TC)], tumor Necrosis factor-alpha (TNF-α), malondialdehyde (MDA) and a significant decrease in adiponectin associated with minor changes in superoxide dismutase (SOD) activity in the obese diabetic rats. Administration of telmisartan, enalapril and or aliskiren caused a significant improvement in serum lipid profile and adiponectin, a minor improvement in SOD activity, a decrease in TNF-α and or MDA. Renin angiotensin blockers significantly improve the metabolism and oxidative dysfunctions in Type 2 DM and aliskiren may show a promising powerful therapy.

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Many hypertensive subjects travel to high altitudes, but little is known on ambulatory blood pressure (ABP) changes and antihypertensive drugs' efficacy under acute and prolonged exposure to hypobaric hypoxia. In particular, the efficacy of angiotensin receptor blockers in this condition is unknown. This may be clinically relevant considering that renin-angiotensin system activity changes at altitude. The HIGHCARE-HIMALAYA study assessed changes in 24 h ABP under acute and prolonged exposure to increasing altitude and blood pressure-lowering efficacy and safety of an angiotensin receptor blockade in this setting.

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The aim of the study was to evaluate an antihypertensive effect of AT1-receptor blocker telmisartan on the rest and exercise blood pressure (BP) in patients suffering from mild and moderate arterial hypertension. Twenty males (mean age 50.9 +/- 6.9) following a 3-week placebo run-in phase were treated by telmisartan 80 mg q.d. Bicycle exercise test and echocardiography was performed at the end of placebo run-in phase and following 12 weeks of treatment. The workload on the bicycle exercise test has been increased by 25 watts every 2 min and stopped at systolic BP (SDP) 240 or diastolic BP (DBP) 130 mmHg. The maximal workload was the same, prior and after 12 weeks of the treatment. Antihypertensive therapy with telmisartan had a favorable effect, i.e. significantly decreased the rest BP--both SBP (152.5 +/- 11.4 mmHg vs. 139.2 +/- 12.3 mmHg, p < 0.001) and DBP (100.0 +/- 4.6 mmHg vs. 88.7 +/- 6.2 mmHg, p < 0.001). There were no significant changes in the heart rate (HR) at rest prior and after telmisartan treatment (71.4 +/- 9.1 b/min vs. 72.2 +/- 10.4 b/min). When repeating the exercise test after 12 weeks of telmisartan treatment we detected the significant decrease of BP at maximal workload, i.e. SBP decreased from 230.9 +/- 11.4 mmHg to 211.3 +/- 12.7 mmHg, p < 0.05 and DBP decreased from 124.6 +/- 7.5 mmHg to 109.7 +/- 9.7 mmHg, p < 0.05. There was a significant decrease in HR (140.6 +/- 13.2 b/min vs. 130.1 +/- 14.2 b/min, p < 0.05) and significant increase in JT interval at maximal workload after telmisartan treatment (0.193 +/- 0.014 sec vs. 0.201 +/- 0.014 sec, p < 0.05). Telmisartan decreased the double product at rest and maximal workload (diff. of 16 x 10(2) mmHg x b/min and 48 mmHg x 10(2) b/min, respectively, p < 0.05).

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The availability of selective, potent, orally active and long acting nonpeptide angiotensin II type 1 (AT1) receptor antagonists has provided the opportunity to obtain the benefits of selectively blocking the renin-angiotensin-aldosterone system at the level of the AT1 receptor that mediates most, if not all, of the important actions of angiotensin II, and avoid the nonspecificity of the angiotensin I converting enzyme inhibitors. Losartan was the first, but by no means remained the only, AT1 receptor antagonist. Numerous other 'sartans' have emerged in the past several years and successfully completed clinical development. With the exception of eprosartan, all others, ie, candesartan, irbesartan, saprisartan, tasosartan, telmisartan, valsartan and zolasartan, are based on medications of losartan's prototypical chemical structure. Among the current AT1 receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280. The mode of (functional) AT1 receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174). It is very likely that slow dissociation kinetics from the AT1 receptor underlie insurmountable antagonism. However, competitive or noncompetitive antagonism does not determine the antihypertensive efficacy, but the slow off-rate may extend the occupancy of the AT1 receptor and thereby lengthen the duration of the antihypertensive effect.

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The present study document that, telmisartan and atorvastatin combination have better renoprotective effects but not with individual drug when compared to the diabetic group. The combination also attenuated the progression of diabetic nephropathy by slowing the proteinuria and microalbuminuria and these effects were confirmed by histopathological analysis.

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Studies have suggested that angiotensin receptor blockers may exert a protective role towards doxorubicin-induced cardiotoxicity, but they have not been extensively investigated in this area. We therefore investigated whether the co-treatment of telmisartan, an angiotensin (Ang II) type-1 receptor blocker, might offer protection against daunorubicin cardiotoxic properties in rats.

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The results did not show an effect of ARBs as a class on increasing cancer incidence in patients with diabetes. However, there was a negative association of losartan but a positive one of candesartan and telmisartan with the overall occurrence of cancer. The underlying mechanism certainly requires further investigation.

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Data for this retrospective cohort study were obtained from Caremark's data warehouse. Patients were included in the analysis if they filled prescriptions for ARBs only, did not receive ARB therapy within the 6 months before the filling of the first ARB prescription (index date), were continuously eligible for benefits for 6 months before the index date, were eligible for prescription benefits for the 12 months following the index date, and were age 20-80 years.

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All patients received medical treatment with telmisartan once daily and were randomized to either electronic compliance monitoring with a reminder and monitoring device or standard therapy for 6 months. Both groups were crossed over after 6 months. Intervention effectiveness was assessed using self-reported compliance and BP.

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This new analysis supports the results of the earlier investigation, in that indapamide SR 1.5 mg/day appeared to be the most effective drug for producing significant reductions in SBP within 8-12 weeks, which is an essential element in optimising cardiovascular prevention among hypertensive patients. The clinical application of these results should take into consideration all the limitations discussed in this analysis.

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Metabolic syndrome is common in patients with hypertension and increases the risk of developing diabetes mellitus. The objective of this study (the MARCADOR study) was to compare the effects of manidipine 20  mg with the extemporary combination of manidipine 10  mg/lisinopril 10  mg, amlodipine 10  mg and telmisartan 80  mg on insulin sensitivity, as well as metabolic, inflammatory and prothrombotic markers, in hypertensive non-diabetic patients with metabolic syndrome.

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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 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.

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Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (ATII)-receptor antagonists suppress the effects of ATII and are effective antihypertensive agents. However, the use of ACE inhibitors is sometimes associated with intolerable side effects (eg, cough, angioedema), and patients may develop a compensatory rise in ATII levels. ATII-receptor antagonists have tolerability profiles similar to that of placebo and inhibit the effects of ATII more completely by blocking the AT1 receptor.

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We report a drug metabolism based analysis of genetic polymorphisms in a Caucasian patient receiving fluvastatin and telmisartan experiencing myotoxicity (myalgia and moderate creatine kinase elevation).

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Telmisartan/amlodipine administered either on the morning or at bedtime can effectively reduce blood pressure. The efficacy of BP lowering is independent of the drug taking time. There is a trend both in better BP lowering and less BP variability when two medications are administered at bedtime.

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Prolongation of P-wave times and increase of P-wave dispersion (PWD) were shown to be independent predictors of atrial fibrillation (AF). Angiotensin II receptor blockers (AARBs) and angiotensin-converting enzyme inhibitors (ACEIs) have beneficial effects on atrial conduction times. However, there are not enough data about the comparative effects of those drugs on PWD.

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The model of acute myocardial infarction (AMI) was established by ligating left anterior descending coronary artery. The surviving rats were divided into AMI (AMI) and telmisartan treatment (telmisartan) groups. And another sham operation group (sham) was designated (n = 8). At the end of study, total heart weight (THW), left ventricular weight (LVW) and weight index were measured; myocardial infarction and inflammatory reactions detected by hematoxylin and eosin and Masson staining; the serum levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNFα), monocyte chemotactic protein-1 (MCP-1), interleukin-6 (IL-6) and interleukin-1 beta (IL-1β) by enzyme-linked immunosorbent assay (ELISA); the levels of transforming growth factor 1 (TGFβ1), collagen I, collagen III and MMP9 mRNA in myocardial tissue by reverse transcription-polymerase chain reaction (RT-PCR); the expressions of TGFβ1, collagen I, collagen III, matrix metallopeptidase 9 (MMP9) and nuclear factor-kappa B (NF-κB) by Western blot.

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In the hepatic uptake of organic anions, organic anion transporting polypeptide (OATP) 1B1 is believed to be mainly involved. We have constructed a set of double-transfected cells coexpressing OATP1B1 and hepatic efflux transporters and characterized the transcellular transport of several anions. Recent reports have also suggested the importance of OATP1B3 in the hepatic uptake of some compounds. However, there is little information about OATP1B3-selective substrate and no good tool for the evaluation of efflux transporters of OATP1B3 substrates. In the present study, we found an OATP1B3-selective substrate and established a novel set of double transfectants expressing OATP1B3. Telmisartan acylglucuronide (tel-glu) is a main metabolite of telmisartan, an angiotensin II receptor antagonist. Tel-glu is recognized by hepatobiliary transport systems and efficiently distributed to liver. Several studies using rat and human hepatocytes and transporter-expressing cells revealed that OATP1B3 was responsible for the hepatic uptake of tel-glu in humans. By using double transfectants expressing OATP1B3, we investigated the transcellular transport of tel-glu as well as estradiol 17beta-d-glucuronide (E(2)17betaG) and cholecystokinin octapeptide (CCK-8) to identify the responsible efflux transporters in their biliary excretion. Vectorial basal-to-apical transport of tel-glu was observed in all kinds of double transfectants expressing OATP1B3. In contrast, basal-to-apical transport of E(2)17betaG and CCK-8 was seen only in the OATP1B3/MRP2 double transfectant compared with OATP1B3-expressing cells. Therefore, the newly established set of double transfectants expressing OATP1B3 combined with OATP1B1-expressing double transfectants can be used as a powerful tool for the rapid identification of hepatic uptake and efflux transporters of organic anions.

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Thirty-five subjects enrolled and completed the protocol. At entry (median or %): age 49 years, 43% female, 77% non-white, 91% non-smokers, CD4+ T cell count 590 cells/mm(3), BMI 31 kg/m(2). AT responses were heterogeneous, with statistically significant losses of median (IQR) total (TAT, 2.9% (-9.8, 0.7), p = 0.03) and subcutaneous (SAT, -2.7% (-9.8, 1.1), p = 0.03) AT, but not VAT (-2.7% (-20.5, 14.2), p = 0.53). Significant decreases in waist circumference and waist:hip ratio occurred (both p<0.001) without BMI or weight changes. In an exploratory analysis, significant increases in TNF-α occurred among female subjects without changes in other inflammatory or metabolic markers. No related adverse events occurred.

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In this double-blind, placebo-controlled trial, we randomly assigned 558 hypertensive participants with ADPKD (15 to 49 years of age, with an estimated glomerular filtration rate [GFR] >60 ml per minute per 1.73 m(2) of body-surface area) to either a standard blood-pressure target (120/70 to 130/80 mm Hg) or a low blood-pressure target (95/60 to 110/75 mm Hg) and to either an angiotensin-converting-enzyme inhibitor (lisinopril) plus an angiotensin-receptor blocker (telmisartan) or lisinopril plus placebo. The primary outcome was the annual percentage change in the total kidney volume.

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Twenty-four-hour, day and night average systolic blood pressure (SBP) and 24-hour, day and night SBP load in the two groups were lowered as compared with before treatment (P < 0.05). The effects of Western medicine combined with SXC on blood pressure depression were better than those of Western medicine (P < 0.05). Western medicine combined with SXC had a significant influence on diastolic blood pressure (DBP) as compared with Western medicine (P < 0.05). The heart rate in the SXC group was reduced as compared with before treatment and the routine group (P < 0.05). Trough to peak ratio in SXC group was higher than that in the routine group, while there was no significant difference in smoothness index between the two groups. Morning surge in blood pressure in the two groups was improved as compared with before treatment (P < 0.05), and there was a significant difference in morning surge in blood pressure between the two groups (P < 0.05).

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Although protection of the kidneys by renin-angiotensin system (RAS) inhibitors is well known, differences in renal protection and the characteristics of RAS inhibitors have not been fully investigated. We randomly allocated 80 patients with hypertension complicated by type 2 diabetes and accompanied by microalbuminuria to 4 groups for treatment with the angiotensin receptor blockers (ARBs) telmisartan, losartan, candesartan and valsartan. Strict anti-hypertensive therapy was performed for 12 months (target blood pressure: lower than 130/80 mmHg), and renal function was compared. At study completion, all groups achieved the hypotensive target and no difference was noted in blood pressure levels. However, influences on renal function differed. In the telmisartan group in particular, the serum creatinine level was unchanged while the urinary albumin level and protein excretion were significantly decreased, displaying a strong renoprotective effect. These findings suggest that, although renal protection is a class effect of ARBs, the effect of telmisartan is particularly strong.

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Telmisartan attenuates liver fibrosis in bile duct-ligated rats via increasing ACE2 expression level.

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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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DPP-4 inhibition on top of ARB treatment significantly reduced urinary albumin excretion and oxidative stress in diabetic eNOS knockout mice. Linagliptin on top of an angiotensin II receptor blocker may offer a new therapeutic approach for patients with diabetic nephropathy.

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micardis dosage maximum 2015-04-04

There is accumulating evidence that RAS inhibitors not only reduce blood pressure, but also exert pleiotropic effects, including a renoprotective effect, amelioration of insulin resistance, reduction in onset of diabetes, and suppression of cardiovascular remodelling,. However, the definite benefit of RAS inhibition in treatment of hypertension with CKD or DM is not conclusive. We previously performed the OlmeSartan and Calcium Antagonists Randomized (OSCAR) study comparing the preventive effect of high-dose ARB therapy versus ARB plus CCB combination therapy on cardiovascular morbidity and mortality in 1164 Japanese elderly hypertensive patients with baseline type 2 diabetes and/or CVD (Am J Med (2012)). This trial showed that there was no significant difference in the incidence of primary events (fatal and non-fatal cardiovascular events and non-cardiovascular death) between ARB plus CCB therapy and high-dose ARB therapy. However, ARB + CCB combination lowered blood pressure more than high-dose ARB, and the combined ARB and CCB therapy reduced the incidence of primary events better than high-dose ARB monotherapy in patients with baseline CVD. Further prespecified CKD subanalysis of the OSCAR study has shown that ARB plus CCB therapy also reduces the incidence of primary events more than high-dose ARB therapy in patients with CKD (eGFR <60 ml/min/1.73 m) (Kidney Int (2013)). Therefore, better blood pressure control by ARB + CCB combination than high-dose ARB monotherapy is associated with lower incidence of cardiovascular events by ARB + CCB combination. Our trial support the notion that better blood pressure control rather than greater inhibition of RAS is important for providing the benefit of ARB-based therapy in elderly hypertensive patients with baseline CKD or CVD.In type 2 diabetic patients, an increased urinary albumin creatinine ratio (UACR) is associated with the development of diabetic nephropathy and macrovascular disease. HOPE sub-study indicates that microalbuminuria is a risk factor for cardiovascular events, all-cause death and hospitalization for congestive heart failure. Further, the increased plasma BNP levels can also predict risk of death and cardiovascular events after adjustment for traditional risk factors. A trial of telmisartan prevention of cardiovascular diseases (ATTEMPT-CVD) was performed to compare the effects of ARB therapy and those of non-ARB standard therapy on UACR and BNP level changes in 1,228 hypertensive patients (Eur J Prev Cardiol (2016)). In this prospective randomized trial, the ARB group had a significant effect on UACR and plasma BNP level changes compared with the non-ARB group, and ARB treatment caused a smaller increase in plasma BNP and a greater decrease in UACR than non-ARB treatment, independently of blood pressure control. These findings suggest the benefit of RAS inhibition in improvement of UACR and BNP.Either DM or CKD is significantly associated with high incidence of dementia or Alzheimer's disease (AD). Therefore, dementia or AD is a key target for treatment of hypertension with baseline DM or CKD. However, the benefit of antihypertensive therapy in prevention of dementia or AD remains to be defined. Interestingly, epidemiological or observational studies show that the use of RAS blockers is associated with lower incidence of dementia or AD. Thus, the potential role of RAS in pathophysiology of dementia or AD is paid much attention. However, the underlying mechanisms are unknown. In preclinical study, we have found that CKD significantly enhances cognitive impairment in a mouse model of AD and RAS inhibition ameliorates cognitive impairment in AD mouse with CKD. Furthermore, we found that brain angiotensin II plays a pivotal role in pathogenesis of AD through oxidative stress, inflammation, or cerebral amyloid angiopathy. Therefore, it is possible that RAS inhibition may be potentially promising for prevention of dementia or AD.In conclusion, although RAS inhibition is beneficial for treatment of hypertension complicated by CKD or DM, appropriate blood pressure control is necessary for the reduction of cardiovascular events by RAS inhibition-based therapy. Furthermore, further clinical and preclinical studies regarding the significance of RAS inhibition in dementia or AD is buy micardis needed to define the potential benefit of RAS inhibition in treatment of hypertension with DM or CKD.

micardis brand name 2016-06-21

One major element of novelty of the 2007 European guidelines on hypertension refers to the concept of risk categorization, with the aim of obtaining a more precise definition of the hypertensive patient. This has lead to identification of different categories of cardiovascular risk, from the low to the very high. Studies performed in the past few years have shown that the very high risk category is quite common buy micardis and it is not unusually accompanied by poor blood pressure control. Results of the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) and the Telmisartan Randomized AssessmeNt Study in ACEI iNtolerant subjects with cardiovascular Disease (TRANSCEND) have allowed us to better define the therapeutic approach to high-risk patients showing the favorable effects of either ramipril or telmisartan on blood pressure control and risk profile. Additionally, these studies have shown that discontinuation of antihypertensive treatment is not a rare phenomenon, which can be at least in part minimized by the use of drugs with a high tolerability profile, such as angiotensin II receptor blockers (ARBs), and more specifically telmisartan. This review article examines in depth the results of the two above-mentioned trials as well as their impact on guidelines on antihypertensive treatment.

micardis hct generic 2017-08-22

The Boehringer Ingelheim trial database was searched for randomised, double-blind studies comparing telmisartan/amlodipine combination therapy with monotherapy. Eight studies were identified. Eight separate analyses were used to compare combination therapy with respective monotherapies at the earliest available time points (weeks 1 buy micardis , 2 and/or 4).

micardis online 2017-07-19

671 patients were selected and 441 were randomised (age: 55 +/- 12 years: 240 men and 201 women). Study populations were the following: the safety population (n = 441, T = 220; P = 221), the intent-to-treat (ITT) population (n = 435, T = 217 and P = 218), and the per protocol population (n = 368, T = 188; P = 180). ITT analysis showed a greater diminution of trough DBP from W0 to W12 with T than with P (T: -6.6 +/- 6.7 mmHg and buy micardis P: -5.1 +/- 7.0 mmHg; p = 0.018 according to ANOVA for repeated measures). Regarding clinic BP, the same results were observed. Likewise, the per-protocol analysis provided similar findings. Doubling dose was significantly less frequent with T (41%; n = 85) than with P (55%; n = 115; p = 0.005). The overall frequency of adverse events was similar in both treatment groups: T = 34% (n = 74) vs p = 32% (n = 70). Most of them were of mild to moderate intensity and transient. As expected, the occurrence of cough was more frequent with P [5% (n = 12), T < 1% (n = 2), p = 0.007].

dosage micardis plus 2015-02-01

This study investigates the beneficial role of lisinopril, an angiotensin converting enzyme inhibitor (ACEI) and telmisartan, an angiotensin receptor blocker (ARB), in intracerebroventricular (i.c.v.) streptozotocin (STZ) induced dementia of Alzheimer's disease (AD) type in mice. This study also aimed to explore the role of PPAR-γ in lisinopril and telmisartan mediated effects in i.c.v. STZ mice. Donepezil served as the positive control in the study. Mice underwent i.c.v. injection buy micardis of STZ. The Morris water maze (MWM) test was employed for assessment of learning and memory. Various biochemical estimations, namely brain acetylcholinesterase (AChE) activity, myeloperoxidase (MPO) activity, nitrite/nitrate and thiobarbituric acid reactive species (TBARS) levels and reduced glutathione (GSH) levels, were also performed. The study showed that i.c.v. STZ significantly impaired learning and memory of the animals along with a significant enhancement in brain AChE, MPO, TBARS, nitrite/nitrate levels and reduction in brain GSH levels. Treatments of lisinopril/telmisartan/donepezil significantly attenuated STZ induced behavioral and biochemical changes. Pre-treatment with bisphenol-A-diglycidyl ether (BADGE), a selective PPAR-γ antagonist, significantly abolished the beneficial effect of lisinopril/telmisartan in i.c.v. STZ treated animals. The results of this investigation document a potential role of PPAR-γ in the beneficial effects of lisinopril and telmisartan in i.c.v. STZ dementia of AD type.

micardis dosage instructions 2015-04-26

Telmisartan and angiotensin-converting enzyme inhibitors (ACEIs) are both effective and widely used antihypertensive drugs targeting renin-angiotensin-aldosterone system. The study aimed to estimate the efficacy and tolerability of telmisartan in comparison with different ACEIs as monotherapy in the treatment of hypertension. Cochrane Central Register of Controlled Trials, PubMed and Embase were searched for relevant studies. A meta-analysis of all buy micardis randomized controlled trials fulfilling the predefined criteria was performed. A random-effect model was used to account for heterogeneity among trials. Twenty-eight randomized controlled trials involving 5157 patients were ultimately identified out of 721 studies. Telmisartan had a greater diastolic blood pressure (DBP) reduction than enalapril (weighted mean difference (WMD) 1.82, 95% confidence interval (CI) 0.66-2.99), ramipril (WMD 3.09, 95% CI 1.94-4.25) and perindopril (WMD 1.48, 95% CI 0.33-2.62). Telmisartan also showed a greater DBP response rate than enalapril (relative risk (RR) 1.15, 95% CI 1.05-1.26), ramipril (RR 1.34, 95% CI 1.11-1.61) and perindopril (RR 1.22, 95% CI 1.05-1.41). There was no statistical difference in DBP reduction or therapeutic response rate between telmisartan and lisinopril (WMD -0.30, 95% CI -0.65 to 0.05; RR 0.99, 95% CI 0.80-1.23, respectively). Telmisartan had fewer drug-related adverse events than enalapril (RR 0.57, 95% CI 0.44-0.74), ramipril (RR 0.44, 95% CI 0.26-0.75), lisinopril (RR 0.70, 95% CI 0.56-0.89) and perindopril (RR 0.52, 95% CI 0.28-0.98). The meta-analysis indicates that telmisartan provides a superior BP control to ACEIs (enalapril, ramipril and perindopril) and has fewer drug-related adverse events and better tolerability in hypertensive patients.

micardis generic 2015-12-27

CD34+/133+ cells (% number of cells per total number of cytometric events) were similar at baseline, being 0.25% (0.17-0.42%) in the FCE vs 0.23% (0.11-0.43%) in the RCE group, and increased at follow-up only in the FCE group to 0.41% (0.22-0.64%), while in the RCE group they were 0.27% (0.11-0.36%) (p=0.009 for the interaction, p=0.07 for the main effect of time). CD34+/KDR+ cells were similar at baseline in the two groups, did not significantly increase over time (p=0.2), and no differential effect of FCE vs RCE over time was seen (p=0.38). buy micardis CRP levels, similar at baseline, were consistently reduced at 20 days after ACS (p=0.001), with no differential effect of FCE vs RCE pts (p=0.74). Variation from baseline to follow-up for both CD34+/133+ and CD34+/KDR+ did not correlate with either baseline CRP or delta CRP.

micardis patient reviews 2015-10-14

At baseline, median urinary albumin-creatinine ratio and eGFR were 6.6 (IQR, 2.9-25.0) mg/mmol and 71.5 (IQR, 58.1-85.9) mL/min/1.73m(2), respectively. After 5.5 years, 704 (32.5%) participants developed albuminuria, 1,194 (55.2%) had a ≥5% annual eGFR decline, 267 (12.3%) had both, and 1,022 (14.8%) had died. Being physically active every day has PAFs of 5.1% (95% CI, 0.5%-9.6%) for CKD and 12.3% (95% CI, 4.9%-19.1%) for death. Among food items, increasing vegetable intake would have the largest impact on buy micardis population health. Considering diet, weight, physical activity, tobacco use, and size of social network, exposure to less than optimum levels gives PAFs of 13.3% (95% CI, 5.5%-20.9%) for CKD and 37.5% (95% CI, 27.8%-46.7%) for death. For the 17.8 million middle-aged Americans with diabetes, improving 1 of these lifestyle behaviors to the optimal range could reduce the incidence or progression of CKD after 5.5 years by 274,000 and the number of deaths within 5.5 years by 405,000.

micardis overdose symptoms 2017-02-05

Diabetic nephropathy, a complex disorder with heterogeneous etiologies, remains one of the most threatening diseases worldwide. There were around 177 million people with diabetes mellitus worldwide, and it has been estimated to be increased to 360 million by buy micardis 2030. Given that about 20-30% of these people develop diabetic nephropathy, the present treatment protocols primarily aim for an efficient glucose and blood pressure control to arrest the initiation and progression of diabetic nephropathy. The treatment of diabetic nephropathy near the beginning at microalbuminuria stage with angiotensin-II-AT1 receptor blockers (ARBs) improves blood pressure control and halts disease progression of diabetic nephropathy. In fact, ARBs exert renoprotective effects independently of their blood pressure lowering effect, as they have direct defensive action on the diabetic kidney. Indubitably, it would be better if an ARB has both glucose-lowering and blood pressure controlling potentials efficiently. Intriguingly, telmisartan has such possessions considering its dual role of AT1 receptor blocking action and peroxisome proliferator-activated receptor gamma (PPARγ) partial agonistic property. The additional PPARγ agonistic potential of telmisartan could make it a distinctive intervention in the ARB class to prevent the progression of diabetic nephropathy through activation of PPARγ-mediated insulin sensitization, and renal anti-inflammatory and anti-oxidant actions. Indeed, telmisartan reduced insulin resistance and glucose intolerance, and halted the progressive renal dysfunction associated with diabetic nephropathy by inhibiting the incidence of albuminuria, and preventing the progression of glomerulosclerosis, renal interstitial inflammation and fibrosis. This review will discuss the current status of therapeutic potentials of telmisartan in treating diabetic nephropathy.

co micardis medication 2016-08-23

Data supporting the use of ARBs for reducing cardiovascular events in patients with essential buy micardis hypertension without compelling indications are limited and inconclusive. More studies are needed before ARBs can be routinely recommended as first-line therapy for hypertension management in patients without other compelling indications.

micardis user reviews 2015-08-06

Angiotensin II type 1 receptor (AT1R) blocker (ARB) has been reported to modify hypertensive cerebrovascular changes; however, it is not clear whether its protective effects are independent of blood pressure. The aim of this study was to clarify the role of buy micardis AT1R-mediated signals in cerebral circulation by the chronic treatment with telmisartan, an ARB, at a dose that did not lower the blood pressure. Male spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) were treated for 4 weeks from 16 weeks of ages with telmisartan (SHR-L: 0.3 mg/kg/day, SHR-H: 3 mg/kg/day, WKY-H: 3 mg/kg/day) or vehicle (SHR-V, WKY-V). Superoxide measured by a chemiluminescent assay or dihydroethidium fluorescence and vascular morphology were examined for the thoracic aorta (Ao), common carotid (CCA), middle cerebral (MCA) and basilar arteries (BA). After 4 weeks of treatment, the blood pressure significantly declined in SHR-H but not in SHR-L in comparison to SHR-V. The lower limit of cerebral blood flow (CBF) autoregulation, evaluated by hemorrhagic hypotension, was significantly lower in SHR-L and SHR-H than SHR-V. In both SHR and WKY, the superoxide levels in the arteries were significantly attenuated by both doses of ARB. ARB also reversed vascular hypertrophy in Ao, CCA and BA and the inward remodeling in MCA. These results suggest that chronic treatment with telmisartan may therefore improve CBF autoregulation with a restoration of the vascular structure and an attenuation of superoxide generation, even at a dose that does not lower the blood pressure.

micardis plus generic 2015-04-01

A total of 20,332 patients were followed for a mean of 2.5 years. Recurrent stroke occurred in 916 patients (9.0%) receiving ASA-ERDP and in 898 patients (8.8%) receiving clopidogrel (hazard ratio, 1.01; 95% confidence interval [CI], 0.92 to 1.11 buy micardis ). The secondary outcome occurred in 1333 patients (13.1%) in each group (hazard ratio for ASA-ERDP, 0.99; 95% CI, 0.92 to 1.07). There were more major hemorrhagic events among ASA-ERDP recipients (419 [4.1%]) than among clopidogrel recipients (365 [3.6%]) (hazard ratio, 1.15; 95% CI, 1.00 to 1.32), including intracranial hemorrhage (hazard ratio, 1.42; 95% CI, 1.11 to 1.83). The net risk of recurrent stroke or major hemorrhagic event was similar in the two groups (1194 ASA-ERDP recipients [11.7%], vs. 1156 clopidogrel recipients [11.4%]; hazard ratio, 1.03; 95% CI, 0.95 to 1.11).

micardis dose maximum 2017-08-05

Treatment with telmisartan not only decreased SBP and DBP levels, but also improved insulin Levitra Headache Remedy resistance and microalbuminuria by T1. Levels of triglycerides significantly decreased and high-density lipoprotein cholesterol increased at T1, whereas total and low-density lipoprotein cholesterol levels were statistically reduced at T3 and T6. Cystatin C and endothelin-1 showed a significant reduction at T1, whereas interleukin-18 decreased at both T3 and T6.

micardis generic name 2015-11-03

Two weeks of therapy Aggrenox Usual Dose with telmisartan led to a significant increase of RPF (from 313 +/- 47 to 348 +/- 69 ml/min/m, P = 0.007) and MRI-ASL kidney perfusion measurements (from 253 +/- 20 to 268 +/- 25 ml/min/100 g, P = 0.020). RPF measurements were related with MRI-ASL kidney perfusion measurements (r = 0.575, P < 0.001). Changes of RPF measurements and changes of MRI-ASL kidney perfusion measurements in response to treatment with telmisartan revealed a close relationship when expressed in absolute terms (r = 0.548, P = 0.015) and in percentage changes (r = 0.514, P = 0.025).

micardis drug class 2017-05-27

Traditional clinical Aldactone 50 Mg trials in hypertension measure the efficacy of antihypertensive drugs but may not fully assess their effectiveness in clinical practice. Community-based trials can provide this information but are limited because usually they are of open-label design and potentially subject to observer bias. Therefore, we used ambulatory blood pressure monitoring (ABPM), an automated and objective measure of blood pressure (BP) to overcome these shortcomings in a large community-based trial.

micardis 120 mg 2015-10-24

The yield of [(11)C]Telmisartan for clinical research use was 16.8 ± 2.9% EOB as decay corrected (n = 8, mean ± SD) in 32-36 min. The radiochemical Sinemet Drug Classification purity of [(11)C]Telmisartan was >97%, and specific activity was higher than 86.3 MBq/nmol.

micardis 8 mg 2017-09-20

In the monotherapy, category angiotensin receptor blockers (ARBs) accounted (24.8%), calcium channel blockers (CCBs) (19.4%), angiotensin converting enzyme inhibitors (ACEIs) (11%), beta blockers (BBs) (2.8%), and diuretics (2%) of the total prescription. Individually, amlodipine was maximally prescribed in 16.4%. 31.6% had double combination, whereas 2.2% and 1% had triple and four drug combinations, respectively. About 3.6% of the prescription contained antihypertensive combination along with other class of drug. ARBs + diuretic were observed in 11%, CCBs + BB 10% and ACEI + diuretic in 2.6% of the total prescriptions. Among the combination therapy amlodipine + atenolol (8.4%), telmisartan + hydrochlorothiazide (6%) and losartan + hydrochlorothiazide (4.4%) were maximally prescribed. 84.21% (P < 0.001) of the prescription showed nonadherence as per recommendations for pre-HT. 100% and 43.25 Zanaflex Dosing % adherence rates were noticed for Stage 1 HT (P < 0.001) and Stage 2 HT (P > 0.05) patients.

micardis 5 mg 2017-01-29

Male Sprague-Dawley rats were randomly assigned to 3 groups. The control group (n = 10) was sham-operated. The animals in the BOO (n = 20) and the telmisartan groups (n = 20) underwent a partial BOO operation. The telmisartan group received telmisartan (3 Uroxatral Reviews mg/kg/d) for 14 days. Cystometry was performed in all 3 groups for 2 weeks after surgery. The expression levels and the cellular distribution of NGF and AT1 receptors were quantified by Western blot analysis and immunofluorescence staining.

micardis maximum dose 2017-06-17

Primary human adipocytes and 3T3-F442A murine adipocytes were Viagra Brand Name incubated with lopinavir or atazanavir boosted with ritonavir, with or without the angiotensin II type-1 receptor (AT1R) blockers (ARBs), irbesartan or telmisartan, and the peroxysome proliferator-activated receptor-gamma (PPAR-gamma) regulators, rosiglitazone and GW9662. Adipose RAS activation and adipocyte functions were evaluated.

micardis hct reviews 2015-01-31

This study compared the effectiveness and tolerability of a single-pill combination (SPC) of telmisartan/hydrochlorothiazide Prandin Dosage Diabetes 80/25 mg (T80/H25) with T80 monotherapy.

micardis generic cost 2015-01-22

Several studies indicate that insulin resistance and diabetes influence sustained viral response in treatment for chronic HCV infection. We describe the case of a relapsed patient with HCV infection who achieved a sustained viral response due to an improvement in insulin resistance through modification of antihypertensive therapy. By improving insulin resistance with telmisartan, an ARB with PPAR gamma agonist propriety, sustained viral response was obtained with the same antiviral therapy. Optimization of comorbidity therapy is useful for improving the possibility of achieving a sustained viral response.

micardis overdose death 2015-12-25

Two separate, randomized, multiple-dose, two-period, one-sequence studies were conducted. In study A, 43 participants received 80 mg of telmisartan orally for 7 days, and were then administered oral chlorthalidone 25 mg for 14 days (days 8-21), coadministered with 80 mg of telmisartan from day 15. In study B, 14 participants received oral chlorthalidone (25 mg) for 13 days, followed by coadministration with 80 mg of telmisartan orally for 7 days.

micardis cost 2016-06-30

Although the prevalence of chronic kidney disease (CKD) is ∼ 30% in the group of people with diabetes, data on interventions in the very early stage of the disease are still missing. Furthermore, the effects of modifiable lifestyle factors such as nutrition on incidence and progression of CKD in patients with diabetes in Europe remain elusive.

micardis 40 mg 2015-03-28

The numbers of LDL-R- and immuno-ApoE-positive neurons increased in both cerebral cortex and hippocampus of SHR/Ve throughout 6, 12, and 18 months of age, compared with age-matched normotensive Wistar rats. On the other hand, telmisartan significantly reduced the numbers of LDL-R- and ApoE immuno-positive neurons in both cerebral cortex and hippocampus, with similar effectiveness in the SHR/Low group without blood pressure (BP) lowering to BP lowering (SHR/High). The decrease of MAP2-positive neuron in SHR/Ve was recovered by telmisartan in both cerebral cortex and hippocampus.

micardis 60 mg 2016-06-18

Our data demonstrate that the effects of Ang II on the collagen gel contraction by adult rat cardiac fibroblasts in serum-free conditions are Ang II type 1(AT(1))-receptor- mediated, because they are abolished by the specific AT(1)-receptor antagonist, telmisartan, and not by the AT(2)-receptor antagonist PD 123319 or by the Ang III antagonist des-Asp(1)-Ile(8)-angiotensin. The Ang III- stimulated contraction of collagen by cardiac fibroblasts is completely blocked by the Ang III receptor antagonist, des-Asp(1)-Ile(8)-angiotensin II, and by telmisartan.

micardis 160 mg 2015-05-23

AT1 receptor blockers (ARB) and in part ACE inhibitors (ACI) potentially exert beneficial effects on atherogenesis independent of AT1 receptor inhibition. These pleiotropic effects might be related to angiotensin II mediated activation of the AT2 receptor. To analyze this hypothesis we investigated the development of atherosclerosis and the role of ACIs and ARBs in apolipoprotein E-deficient (ApoE(-/-)) mice and in ApoE/AT1A receptor double knockout mice (ApoE(-/-)/AT1A(-/-)). ApoE(-/-) mice and ApoE(-/-)/AT1A(-/-) mice were fed cholesterol-rich diet for 7 weeks. Vascular oxidative stress, endothelial dysfunction, and atherosclerotic lesion formation were evident in ApoE(-/-) mice, but were markedly reduced in ApoE(-/-)/AT1A(-/-) mice. Concomitant treatment of ApoE(-/-)/AT1A(-/-) mice with either telmisartan or ramipril had no additional effect on blood pressure, vascular oxidative stress, AT2 receptor expression, and endothelial function. Remarkably, atherosclerotic lesion formation was increased in ramipril treated ApoE(-/-)/AT1A(-/-) mice compared to untreated ApoE(-/-)/AT1A(-/-) mice whereas pharmacological AT1 receptor inhibition with telmisartan had no additional effect on atherogenesis. Moreover, chronic AT2 receptor inhibition with PD123,319 significantly increased plaque development in ApoE(-/-)/AT1A(-/-) mice. In additional experiments, direct AT2 receptor stimulation reduced atherogenesis in ApoE(-/-)/AT1A(-/-) mice. Taken together, our data demonstrate a relevant antiatherosclerotic role of the AT2 receptor in atherosclerotic mice and provide novel insight in RAS-physiology.

micardis and alcohol 2016-02-25

Glomerular volume was significantly increased in the diabetic rats, and there was heterogeneity in the glomerular volumes. The diameter ratio of the afferent to efferent arterioles significantly increased, and there was increased glomerular permeability in the diabetic rats compared with the control rats. Telmisartan treatment reduced glomerular permeability without affecting glomerular volume.