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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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The selection criteria were deliberately broad due to there being few clinical trials in children. We included randomised controlled trials (RCTs) of at least two weeks duration comparing antihypertensive agents either as monotherapy or combination therapy with either placebo or another medication, or comparing different doses of the same medication, in children with hypertension. Hypertension was defined as an average (over a minimum of three readings) systolic or diastolic blood pressure (or both) on the 95(th) percentile or above for age, height and gender.

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The benefits of blood pressure control on the risks of major cardiovascular events are well established. In clinical trials conducted in patients with mild-to-moderate hypertension, the angiotensin II receptor blocker (ARB) telmisartan has been shown to provide reduction of blood pressure throughout the 24-h dosing interval. Clinical trials have also demonstrated that ARBs are effective agents in reducing the risk of cardiovascular mortality, stroke, heart failure and new-onset atrial fibrillation. Recently, the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) study established that telmisartan reduces morbidity and mortality in a broad cross-section of patients at high risk for heart and vascular events, to an extent similar to that of the angiotensin-converting enzyme inhibitor ramipril. In addition, ONTARGET demonstrated that telmisartan is somewhat better tolerated than ramipril. Attributes such as effective blood pressure lowering, tolerability and convincing outcomes data mean that ARBs satisfy the requirements for first-line antihypertensive agents.

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Our results suggest that TLM has the potential to reduce mortality, LVH, and LVEDP and that enhanced sympathoinhibition by reduction of ROS in the RVLM might be one of the mechanisms contributing to the beneficial actions of TLM in a model of rats with severe hypertension and heart failure.

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The oral clearance (CL/F) was found to be associated with age, dose and alcohol consumption, but neither related to serum creatinine nor smoking history. The volume of distribution for the central compartment was related to age and dose, and the volume of distribution for the peripheral compartment was related to body weight and gender. The absorption rate constant (Ka) and the absorption lag time were described as function of dose. The CL/F decreased with advanced age. The CL/F decreased and Ka increased with higher dose, reflecting the super-proportional increase in the plasma levels of telmisartan. The AUC and C(max) values predicted by the present PPK model were well consistent with the observed values. The means of parameter estimates obtained with 200 bootstrap replicates were within 95-111% of the final parameter estimates from the original data set.

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After the active dose, telmisartan reduced the BP during the last 6 h of the dosing period by -11/-7.6 +/- 0.8/0.6 mm Hg compared to -8.7/-5.8 +/- 0.8/0.6 mm Hg on valsartan (P = .02 for systolic BP and.01 for diastolic BP). On the day of the missed dose, telmisartan reduced the early morning BP by -9.0/-6.3 +/- 0.7/0.6 mm Hg versus -7.4/-5.1 +/- 0.7/0.4 mm Hg on valsartan (P = .09 for systolic BP and.06 for diastolic BP). On the day of the missed dose, reductions in 24-h average BP for the two antihypertensive agents were -10.3/-6.9 mm Hg for telmisartan versus -8.7/-5.9 mm Hg for valsartan (P = .06 for systolic BP and.056 for diastolic BP).

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Two-hundred and twenty-four client-owned adult cats with CKD.

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In clonal animal cells, certain angiotensin receptor blockers (ARB) activate the peroxisome proliferator-activated receptor-gamma (PPARgamma). The aim of this work was to validate that observation in human cells and humans.

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Visfatin was found expressed in cardiomyocytes as well as cardiac fibroblasts, and there was no significant difference at the mRNA and protein levels of visfatin. Ang II treatment induced the increased expression of visfatin and brain natriuretic peptide in a dose- and time-dependent manner in cardiomyocytes, and pretreatment with AT1-R antagonist telmisartan completely blocked Ang II-induced visfatin expression increasement. The increased visfatin expression was also blocked by the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway inhibitor AG490.

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Six phase 3, double-blind studies of 8 weeks' duration that assessed the T/H12.5 SPC and T40 or T80 monotherapy, were included in the analysis. Data was pooled separately for the two T40 non-responder studies (T40 NR group, two T80 non-responder studies (T80 NR group), and the two factorial design dose-response studies (FD-DR group).

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The objective of the present work was to obtain pH independent and improved dissolution profile for a poorly soluble drug, telmisartan using liquisolid compacts. Liquisolid compacts were prepared using Transcutol HP as vehicle, Avicel PH102 as carrier, and Aerosil 200 as a coating material. The formulations were evaluated for drug excipient interactions, change in crystallinity of drug, flow properties, and general quality control tests of tablets using Fourier transform infrared (FTIR) spectroscopy, differential scanning calorimetry (DSC), X-ray diffraction (XRD), angle of repose, and various pharmacopoeial tests. In vitro dissolution studies were performed at three pH conditions (1.2, 4.5 and 7.4). Stability studies were performed at 40°C and 75% RH for three months. The formulation was found to comply with Indian pharmacopoeial limits for tablets. FTIR studies confirmed no interaction between drug and excipients. XRD and DSC studies indicate change/reduction in crystallinity of drug. Dissolution media were selected based on the solubility studies. The optimized formulation showed pH independent release profile with significant improvement (P < 0.005) in dissolution compared to plain drug and conventional marketed formulation. No significant difference was seen in the tablet properties, and drug release profile after storage for 3 months.

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This study aimed to clarify the impact of telmisartan on fat distribution and insulin sensitivity in the metabolic syndrome. In this open-label, prospective, randomized study, patients with the metabolic syndrome (waist circumference: men >or= 85 cm, women >or= 90 cm) were treated either with amlodipine (n = 26) or with telmisartan (n = 27) for 24 weeks, and fat distribution and insulin sensitivity were determined.

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Baseline alanine aminotransferase (ALT), aspartate aminotransferase (AST), insulin resistance index, components of metabolic syndrome, age, and sex were similar in both groups. At the end of study, NAS improvement in TL and L groups was 2.15 ± 1.66 and 1.10 ± 0.57 (P = 0.017) and fibrosis improvement was 0.65 ± 0.93 and -0.30 ± 0.48 (P = 0.001), respectively. NAS improved by ≥ 2 in 13 (65%) and 2 (20%) patients and fibrosis score improved by ≥ 1 in 8 (40%) patients and none of the patients in TL group and L group, respectively. Telmisartan and life style modification could improve steatosis, ballooning, lobular inflammation, and fibrosis. Life style modification could improve ballooning only, but fibrosis deteriorated. TL group showed improvement in NAS and fibrosis score [P value: 0.035; odds ratio (OR) =92.07, confidence interval (CI) =1.39-6106] to the level of response by regression analysis. Weight reduction and improvement of metabolic syndrome did not influence the response. There were similar minor adverse events in both groups.

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Vascular responsiveness to vasoconstrictors is known to be attenuated in haemorrhagic shock. In this study we assessed the temporal development and the underlying mechanisms of haemorrhage-induced vascular hyporeactivity to pressor agents.

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Previous studies established that a single daily dose of olmesartan remains effective for the entire 24 h without alteration of the day-night blood pressure (BP) pattern. On the other hand, the administration of valsartan or telmisartan at bedtime, as opposed to upon wakening, improves the sleep-time relative BP decline toward a greater dipper pattern without loss of 24 h efficacy. Yet to be determined is whether this administration-time-dependent efficacy is a class-related feature, characteristic of all angiotensin-receptor-blocker (ARB) medications. We studied 123 grade 1 and 2 hypertensive patients, 46.6+/-12.3 yrs of age, randomly assigned to receive olmesartan (20 mg/day) as a monotherapy either upon awakening or at bedtime for three months. BP was measured by ambulatory monitoring for 48 consecutive hours before and after treatment. The 24 h BP reduction was similar for both treatment times. Administration of olmesartan at bedtime, however, was significantly more efficient than morning administration in reducing the nocturnal BP mean. The sleep-time relative BP decline was slightly reduced with olmesartan ingestion upon awakening but significantly increased with ingestion at bedtime, thus reducing the prevalence of non-dipping from baseline by 48%. Olmesartan administration at bedtime, as opposed to in the morning, improved the awake/asleep BP ratio toward a greater dipper pattern without loss of 24 h efficacy. Nocturnal BP regulation was significantly better achieved with bedtime as compared to morning dosing of olmesartan. These effects are comparable to those previously reported for valsartan and telmisartan, thus suggesting that they may be class-related features of ARB medications in spite of differences in their half-life kinetics. These administration-time-dependent effects should be taken into account when prescribing ARB medications for treatment of essential hypertension.

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If the association between diet and these endpoints is causal, then optimizing diet quality in individuals with diabetes who have no CKD or very early CKD would have substantial population benefits in terms of prevention of CKD incidence or progression and mortality in this high-risk population.

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According to Akaike's information criterion values, the proposed indirect response model provided a more appropriate and good-fitting PK/PD characterization of telmisartan than the effect-compartment link model in SH rats.

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Twenty-week telmisartan treatment significantly and dose-dependently increased (18)F-FDG levels in the blood (percentage injected dose per gram of tissue normalized by animal body weight: low, 0.13 ± 0.03 [P < 0.0083]; moderate, 0.15 ± 0.01 [P < 0.0083]; high, 0.15 ± 0.03 [P < 0.0083], vs. control, 0.09 ± 0.01). Significantly increased (18)F-FDG levels in organs were observed in mice in the moderate- and high-dose groups but not in the low-dose group. The plasma BUN and creatinine levels also dose-dependently increased, but they were within the reference ranges (for BUN: low, 27.00 ± 4.42 mg/dL; moderate, 28.40 ± 2.70 mg/dL; high, 39.22 ± 6.91 mg/dL [P < 0.0083], vs. control, 22.40 ± 2.80 mg/dL. For creatinine: low, 0.28 ± 0.11 mg/dL; moderate, 0.40 ± 0.07 mg/dL [P < 0.0083]; high, 0.51 ± 0.09 mg/dL [P < 0.0083], vs. control, 0.18 ± 0.04 mg/dL). The blood (18)F-FDG level positively correlated with plasma BUN (r = 0.48, P < 0.01) and creatinine (r = 0.61, P < 0.01) levels. The (18)F-FDG levels in the blood and organs returned to baseline 3 wk after cessation of telmisartan treatment. Autoradiography indicated that renal (18)F-FDG excretion was attenuated by telmisartan treatment and was reversed after treatment cessation.

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Pigment epithelium-derived factor (PEDF) is a natural extracellular component of the retina with neuronal differentiating activity. Decreased levels of PEDF in the mammalian eye have been shown to participate in proliferative diabetic retinopathy. In addition, we have recently found in in vitro experiments that PEDF protected against pericyte apoptosis, the earliest histopathological hallmark of diabetic retinopathy. These observations suggest that the loss of PEDF in the mammalian eye plays an important role in the development and progression of diabetic retinopathy. However, the functional role of endothelial cell (EC)-derived PEDF in pericyte survival and the regulation of PEDF gene expression remain to be elucidated. In this study, we examined the effects of anti-PEDF antibody (Ab) on the viable cell number of cocultured pericytes with microvascular ECs. We further studied the effects of angiotensin II (Ang II) on PEDF gene expression in ECs. Anti-PEDF Ab significantly inhibited the growth-stimulating effects of cocultured ECs on pericytes. Furthermore, Ang II significantly decreased PEDF mRNA levels in ECs, which was completely reversed by an Ang II type 1 receptor blocker, telmisartan. Our present results suggest that PEDF is an EC-derived mitogen or survival factor for retinal pericytes. Suppression by Ang II of the EC-derived PEDF may be involved in exacerbation of diabetic retinopathy in patients with hypertension.

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Cell proliferation was significantly inhibited by ADMA. ADMA increased intracellular ROS generation in BRCECs. The increased ROS production induced by ADMA was markedly inhibited by the angiotensin II receptor-blocker telmisartan, the angiotensin-converting enzyme inhibitor benazepril, the reduced form of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenyliodonium (DPI), or the antioxidant and free-radical scavenger N-acetyl-L-cysteine (NAC). ADMA significantly increased horseradish peroxidase (HRP) permeability in BRCECs. Benazepril, telmisartan, DPI, and NAC downregulated cell permeability. ADMA markedly upregulated ICAM-1 expression in BRCECs, which were downregulated by telmisartan, DPI, and NAC. ADMA significantly downregulated occludin expression in BRCECs. Benazepril and telmisartan upregulated occludin expression in BRCECs exposed to ADMA.

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Low dose TMS and its combination with metformin normalizes depressive mood, reduces pro-inflammatory mediators and ameliorates the HPA axis function; thereby providing beneficial effects in DID.

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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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In total, 840 patients were randomized. At week 10, T/HCTZ provided significantly greater reductions versus V/HCTZ in the last 6 hours mean ABP (differences in favour of T/HCTZ: SBP 3.9 mm Hg, p < 0.0001; DBP 2.0 mm Hg, p = 0.0007). T/HCTZ also produced significantly greater reductions than V/HCTZ in 24-hour mean ABP (differences in favour of T/HCTZ: SBP 3.0 mm Hg, p = 0.0002; DBP 1.6 mm Hg, p = 0.0006) and during the morning, daytime and night-time periods (p < 0.003). Both treatments were well tolerated.

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Nebivolol is a cardioselective beta-blocker that has been reported to be efficacious and well tolerated for achieving BP control in patients with hypertension. Preliminary evidence suggests a potential for reduced mortality in patients with heart failure.

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The Candesartan Cooperative Research of Therapy Design for Early Morning Hypertension in CHIBA was designed to investigate whether switching from angiotensin II receptor blockers (ARBs) except candesartan to candesartan might be effective in Japanese patients with morning hypertension. Seventy-eight mild to moderate hypertensive patients, who were treated with the standard doses of ARBs except candesartan (losartan, 50 mg; valsartan, 80 mg; telmisartan, 40 mg; or olmesartan, 20 mg), were entered into 12-week treatment period with candesartan 8 mg according to a multicenter, open-label design. Morning and office blood pressures (BPs) were significantly reduced (morning, -10.1 ± 10.5/-4.5 ± 8.4 mm Hg; office, -13.1 ± 17.3/-6.2 ± 11.3 mm Hg) after medication change. Target BPs (morning BPs ≤ 135/85 mm Hg and office BPs ≤ 140/90 mm Hg) achievement rates were 42.9% in the morning and 64.3% at office. No adverse events were recognized in all patients. Candesartan treatment significantly reduced the morning and office BPs compared with other ARBs in Japanese patients with morning hypertension.

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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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HIV-infected persons are at increased cardiovascular disease (CVD) risk, but traditional CVD therapies are understudied in this population. Telmisartan is an angiotensin receptor blocker (ARB) and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist that improves endothelial function and cardiovascular mortality in HIV-uninfected populations. We assessed the effects of telmisartan on endothelial function in older HIV-infected persons at risk for CVD in a small pilot study.

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micardis reviews 2016-03-09

Of 651 potentially relevant reports, 15 satisfied the inclusion criterion. While visceral fat area was significantly lower in the telmisartan group than in buy micardis the control group (weighted mean difference = -18.13 cm(2), 95% C.I. = -27.16 to -9.11, Pχ(2) = 0.19, I(2) = 41%), subcutaneous fat area was similar (weighted mean difference =2.94 cm(2), 95% C.I. = -13.01 to 18.89, Pχ(2) = 0.30, I(2) = 17%). Total cholesterol levels were significantly different between the groups (standardized mean difference = -0.24, 95% C.I. = -0.45 to -0.03, Pχ(2) = 0.0002, I(2) = 67%).

dosage micardis hct 2016-04-30

Atherosclerotic plaques develop at arterial regions subjected to non-uniform shear stress, and are initiated by increased leukocyte-endothelial interactions. Here we applied the in vitro model of arterial bifurcations to buy micardis investigate whether telmisartan, an anti-inflammatory angiotensin II receptor blocker with PPAR-gamma activating ability, prevents monocyte recruitment by endothelium.

micardis reviews comments 2015-11-05

The additional treatment with AT1 receptor antagonists resulted in an increase in the cardiac output and a decrease in the peripheral resistance. This beneficial effect may be due to the additional property of sartans to block buy micardis the interaction of locally and non-ACE-generated angiotensin II with their respective vascular and myocardial AT1 receptors.

micardis 5 mg 2017-09-28

Telmisartan, an buy micardis angiotensin receptor blocker also called metabosartan, is a promising solution for preventing cognitive decline or the incidence of dementia.

micardis generic availability 2017-07-30

Male, 12-14-weeks-old C57BL6/J and C57BL6/J (IL-6-/-) mice were used. To assess short term changes, a transient reversible ischemia model was buy micardis utilized. Heart failure was caused by ligation of anterior descending coronary artery. The presence of systolic dysfunction was confirmed by echocardiography and left ventricular ANP RNA expression. Molecular analysis was performed on left ventricular samples from animals sacrificed 12-14 weeks after infarction. Western blotting and QT-PCR were used to investigate abundance of CCN proteins and RNAs, respectively.

micardis drug 2015-04-17

Therapy with telmisartan initiated soon after an ischemic stroke and continued for 2.5 years did not significantly lower the rate of recurrent stroke, major cardiovascular buy micardis events, or diabetes. (ClinicalTrials.gov number, NCT00153062.)

micardis overdose death 2015-02-16

Telmisartan and losartan buy micardis , angiotensin II type 1 (AT1) receptor antagonists, are used to manage hypertension. We previously reported that telmisartan, a partial agonist of peroxisome proliferator-activated receptor-γ (PPAR-γ), exhibited stronger vasoprotection than the same dose of losartan in normotensive chronic kidney disease (CKD) rats. We investigated whether telmisartan could inhibit vascular dysfunction in hypertensive CKD rats, via both AT1 receptor blockade and PPAR-γ activation, more effectively than losartan, which decreased blood pressure to a similar extent as telmisartan.

micardis 20 mg 2017-04-10

To investigate the effect of perindopril, amlodipine and telmisartan buy micardis on improving the artery stiffness in patients with hypertension.

micardis generic alternative 2015-11-23

This multicentre, open-label extension study to four controlled trials involved 888 patients with mild-to-moderate primary hypertension. Patients received telmisartan 40-80 mg once daily with add-on hydrochlorothiazide (HCTZ; 12.5-25 mg) if necessary and/or other antihypertensives to achieve diastolic blood pressure (DBP) control (<90 mmHg). Treatment continued for up to 4 years. At treatment end, 578 (65.1%) patients were on telmisartan monotherapy, 106 (11.9%) were on telmisartan + HCTZ 12.5 mg, 101 (11.4%) were on telmisartan + HCTZ 25 mg, and 103 (11.6%) were on telmisartan + another antihypertensive + HCTZ. Overall, 84.4% (746/884) patients achieved DBP control. The buy micardis highest proportion of responders was in the telmisartan monotherapy (40 or 80 mg) treatment category (89.0% 1,511/574 patients]). The mean change in systolic blood pressure (SBP)/DBP from the previous trial baseline to last available trough was -21.2/-17.3 mmHg with telmisartan alone, -24.6/-16.7 mmHg with telmisartan + HCTZ, and - 18.7/-14.9 mmHg with telmisartan + another antihypertensive +/- HCTZ. Most adverse events were of mild-to-moderate intensity and unrelated to treatment. The proportions of patients discontinuing the study due to adverse events, by treatment at onset, were 7.3% (65/888) with telmisartan monotherapy, 6.6% (20/304) with telmisartan + HCTZ and 2.9% (3/103) with telmisartan + another antihypertensive +/- HCTZ. There were 15 deaths during the study, but none was considered drug related. Thus, telmisartan alone or in combination with other antihypertensives achieved and maintained clinically relevant reductions in DBP and SBP. This long-term analysis supports the favourable efficacy and safety profile of telmisartan both as monotherapy and in combination with other antihypertensive drugs.

co micardis medication 2016-06-20

In this multicentre, prospective, randomized, open-label, blinded-endpoint (PROBE) study, the efficacy of 12 weeks' treatment with once-daily telmisartan 40-80 mg and enalapril 10-20 mg was evaluated using ambulatory blood pressure monitoring (ABPM) in 522 patients with mild-to-moderate essential hypertension. Patients were titrated to the higher dose of study drug at week 6 if mean seated diastolic blood pressure (DBP) was > or = 90 mmHg. The primary endpoint was the change from baseline in ambulatory DBP in the last 6 h of the 24-h dosing interval after 12 weeks' treatment. Telmisartan and enalapril buy micardis produced similar reductions from baseline in DBP and systolic blood pressure (SBP) over all ABPM periods evaluated (last 6 h, 24-h, daytime and night-time). Telmisartan produced a significantly greater reduction in mean seated trough DBP, measured unblinded with an automated ABPM device in the clinic, amounting to a difference of -2.02 mmHg (P < 0.01). A significantly greater proportion of patients achieved a seated diastolic response with telmisartan than enalapril (59% versus 50%; P < 0.05), also measured with the same ABPM device. Both treatments were well tolerated. Compared with telmisartan, enalapril was associated with a higher incidence of cough (8.9% versus 0.8%) and hypotension (3.9% versus 1.1%). Therefore, telmisartan may provide better long-term compliance and, consequently, better blood pressure control than enalapril.

micardis y alcohol 2015-07-02

A cell proliferation assay buy micardis was performed using the novel tetrazolium compound 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium and an electron coupling reagent. Intracellular ROS levels were determined using the fluorescent probe CM-H(2)DCFDA. Horseradish peroxidase was used for a permeability assay. ICAM-1 and tight-junction protein occludin were assessed by western blotting and quantitative real-time PCR.

micardis plus generic 2015-11-28

A total of 21,750 new diabetic patients who started antihypertensive treatment were identified from the Taiwan National Health Insurance claims database during the period from July 1, 2000, to December 31, 2000. As of December 31, 2007, patients with incident cancer were included as cases and up to four age- and sex-matched controls were selected by risk-set sampling. Logistic buy micardis regression models were applied to estimate the odds ratios (ORs) and 95% CIs between ARB use and cancer incidence, adjusted for other types of antihypertensive drugs, insulin, oral hypoglycemic agents, statins, and underlying diseases.

micardis maximum dose 2016-12-13

The combination of rosuvastatin with sartans of different peroxisome proliferator receptor-γ activating capacity was buy micardis associated with a decrease in levels of plasma 8-iso-PGF2a. This decrease reached significance only in the telmisartan group.

micardis cost 2017-11-26

This article reviews the clinical pharmacology of nebivolol and its efficacy and safety profile in clinical studies of hypertension (the US Food buy micardis and Drug Administration-approved indication) and heart failure (off-label use).

micardis 120 mg 2016-03-25

Angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) have been used to normalize the blood Lexapro Alcohol pressure and the dipping pattern in patients with type 1 diabetes mellitus (T1DM) and nephropathy. However, there are no data on the effect of the dual blockade on the dipping pattern in these subjects. We therefore, carried out this study to evaluate the effect of administrating an ACEI followed by ARB in the optimum doses in T1DM patients with nephropathy on 24 h blood pressure (BP) profile and nocturnal dipping pattern.

micardis dosage 2017-10-15

We investigated the ability of angiotensin II type 1 (AT1) receptor blockers with peroxisome proliferator-activated receptor (PPAR)-gamma agonist activity (telmisartan and irbesartan) and AT1 receptor blockers devoid of PPARgamma agonist activity (eprosartan and valsartan) to inhibit vascular cell proliferation studied in the absence of angiotensin II stimulation. Telmisartan and, to a lesser extent, irbesartan inhibited proliferation of human aortic vascular smooth muscle cells in a dose-dependent fashion, whereas eprosartan and valsartan did not. To investigate the role of PPARgamma in the antiproliferative effects of telmisartan, we studied genetically engineered NIH3T3 cells that express PPARgamma. Pioglitazone inhibited proliferation of NIH3T3 cells expressing PPARgamma but had little effect on control NIH3T3 cells that lack PPARgamma. In contrast, telmisartan inhibited proliferation equally in NIH3T3 with and without PPARgamma. Valsartan failed to inhibit proliferation of either cell line. In addition, telmisartan inhibited proliferation equally in aortic smooth muscle cells derived from mice with targeted knockout of PPARgamma Augmentin Uti Dosage in the smooth muscle and from control mice, whereas valsartan had no effect on cell proliferation. Telmisartan, but not valsartan, reduced phosphorylation of AKT but not extracellular signal-regulated kinase otherwise induced by exposure to serum of quiescent human smooth muscle cells, quiescent mice smooth muscle cells lacking PPARgamma, or quiescent Chinese hamster ovary-K1 cells lacking the AT1 receptor. In summary, the antiproliferative effects of telmisartan in the absence of exogenously supplemented angiotensin II involve more than just AT1 receptor blockade and do not require activation of PPARgamma. It might be postulated that inhibition of AKT activation is a mechanism mediating the antiproliferative effects of telmisartan, including in cells lacking AT1 receptors or PPARgamma.

micardis dosage maximum 2017-07-25

Blood pressure level markedly reduced in four groups. There was significantly synergistic effect of combination of telmisartan with rosuvastatin on reducing carotid imtima-media thickness (IMT), Th17 cells frequency, IL-17, IL-6, IL-23, tumor necrosis factor (TNF)-α, expression of retinoic acid receptor-related orphan receptor (ROR)γt mRNA, Th17/Treg ratio, IL-1β, IL-2, IFN-γ, hsCRP, and MCP-1, and increasing Treg cells frequency, IL-10, transforming growth factor(TGF)-β1, and expression Trental Dosage of forkhead/winged helix transcription factor (Foxp3) mRNA (all P<0.05). Change rate of IMT statistical positively related to descent rates of Th17 cells frequency, IL-17, IL-6, IL-23, TNF-α, expression of RORγt mRNA, Th17/Treg ratio, IL-1β, IL-2, IFN-γ, hsCRP, and MCP-1, and negatively related to increased rates of Treg frequency, IL-10, TGF-β1, and expression of Foxp3 mRNA, respectively (all P<0.05).

micardis drug class 2017-11-27

Treatment with Perindopril showed that mean baseline values for blood urea, serum creatinine and creatinine clearance in newly diagnosed and old hypertensive patients were 30.88, 1.37, 64.09 and 33.68, 1.53, 55.98, respectively. After study period these values were 32 Vermox 100mg Cost .24, 1.40, 63.97 and 29.80, 1.46, 59.23 respectively (p value > 0.05). Treatment with telmisartan showed that mean baseline values of blood urea, serum creatinine and creatinine clearance in both group of patients were 30.88, 1.52, 59.31, and 31.72, 1.40, 65.67, respectively. After treatment these values in both groups were 31.92, 1.43, 62.66; and 32.20, 1.46, 61.70, respectively (p value > 0.05).

micardis overdose 2017-02-15

Multidrug resistance (MDR), usually mediated by overexpression of efflux transporters such as P-gp, ABCG2 and/or MRP1, remains a major obstacle hindering successful cancer chemotherapy. There has been great interest in the development of inhibitors towards these transporters to circumvent resistance. However, since the inhibition of transporter is not specific to cancer cells, a decrease in the cytotoxic drug dosing may be needed to prevent excess toxicity, thus undermining the potential benefit brought about by a Lanoxin Brand Name drug efflux inhibitor. The design of potent MDR modulators specific towards resistant cancer cells and devoid of drug-drug interactions will be needed to effect MDR reversal.

micardis overdose symptoms 2016-12-08

This article seeks to objectively review the clinical trial evidence to determine whether angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin-receptor Oxytrol Medication Interactions blockers (ARBs) have special cardiovascular protective effects.

micardis hct dosage 2015-07-10

This study compared the cardiovascular and renal effects of long-term telmisartan (3 and 10 mg/kg/day)and lisinopril (10 mg/kg/day) in an animal model combining hypertension and diabetes mellitus. It was a parallel-group study of diabetic, spontaneously hypertensive rats (SHR), treated with control or active treatment for eight months. A non-diabetic SHR control group was run in parallel. Diabetes was induced by streptozotocin (45 mg/kg i.v.) in SHRs aged 9-10 weeks. Animals were treated with telmisartan (3 or 10mg/kg/day), lisinopril (10 mg/kg/day) or vehicle. Plasma glucose levels, blood pressure (BP), and urinary protein and albumin excretion were measured monthly. Telmisartan treatment significantly reduced BP of diabetic SHRs in a dose-dependent manner (p<0.05, low-dose, n= 18; p<0.01, high-dose, n=15). The BP reduction in the lisinopril group was similar to that in the telmisartan 10 mg/kg/day group. Compared with non-diabetic SHRs, untreated diabetic SHRs developed severe proteinuria and albuminuria over the experimental period (p<0.01). In diabetic SHRs, proteinuria and albuminuria were dose-dependently and significantly attenuated by treatment with telmisartan (p<0.01 with the higher dose) and lisinopril (p<0.01). Compared with Sinequan Tablets the untreated diabetic SHRs, cardiac hypertrophy was significantly reduced after treatment with both doses of telmisartan and with lisinopril. Telmisartan, 10 mg/kg/day, but not lisinopril, significantly attenuated the diabetes-induced increase in glomerular volume. In conclusion, telmisartan, 10 mg/kg/day, is at least as beneficial as lisinopril, 10 mg/kg/day, in lowering BP, reducing cardiac hypertrophy and attenuating renal excretion of protein and albumin in this model.

micardis 8 mg 2015-08-06

Angiotensin II receptor blockers (ARBs) represent a new class of effective and well tolerated orally active antihypertensive agents. Recent clinical trials have shown the added benefits of ARBs in hypertensive patients (reduction in left ventricular hypertrophy, improvement in diastolic function, decrease in ventricular arrhythmias, reduction in microalbuminuria, and improvement in renal function), and cardioprotective effect in patients with heart failure. Several large long-term studies are in progress to assess the beneficial effects of ARBs on cardiac hypertrophy, renal function, and cardiovascular and cerebrovascular morbidity and mortality in hypertensive patients with or without diabetes mellitus, and the value of these drugs in patients with heart disease and diabetic nephropathy. The ARBs specifically block the interaction of angiotensin II at the AT1 receptor, thereby relaxing smooth muscle, increasing salt and water excretion, reducing plasma volume, and decreasing cellular hypertrophy. These agents exert their blood pressure-lowering effect mainly by reducing peripheral vascular resistance usually without a rise in heart rate. Most of the commercially available ARBs control blood pressure for 24 h after once daily dosing. Sustained efficacy of blood pressure control, without any evidence of tachyphylaxis, has been demonstrated after long-term administration (3 years) of some of the ARBs. The efficacy of ARBs is similar to that of thiazide diuretics, beta-blockers, angiotensin-converting enzyme inhibitors or calcium channel blockers in patients with similar degree of hypertension. Higher daily doses, dietary salt restriction, and concomitant diuretic or ACE inhibitor administration amplify the antihypertensive effect of ARBs. The ARBs have a low incidence of adverse effects (headache, upper respiratory infection, back pain, muscle cramps, fatigue and dizziness), even in the elderly patients. After the approval of losartan, five other ARBs (candesartan cilexetil, eprosartan, irbesartan, telmisartan, and valsartan) and three combinations with hydrochlorothiazide (irbesartan, losartan and valsartan) have been approved as antihypertensive agents, and some 28 compounds are in various stages of development. The ARBs are non-peptide compounds with varied structures; some (candesartan, losartan, irbesartan, and valsartan) have a common tetrazolo-biphenyl structure. Except for irbesartan, all active ARBs have a carboxylic acid group. Candesartan cilexetil is a prodrug, while losartan has a metabolite (EXP3174) which is more active than the parent drug. No other metabolites of ARBs contribute significantly to the antihypertensive effect. The variation in the molecular structure of the ARBs results in differences in the binding affinity to the receptor and pharmacokinetic profiles. The differences observed in lipid solubility, absorption/distribution, plasma protein binding, bioavailability, biotransformation, plasma half-life, and systemic elimination influence the time of onset, duration of action, and efficacy of the ARBs. On the basis of Cipro 200 Mg the daily mg dose, the antihypertensive potency of the ARBs follows the sequence: candesartan cilexetil > telmisartan approximately = losartan > irbesartan approximately = valsartan > eprosartan. After oral administration, the ARBs are rapidly absorbed (time for peak plasma levels = 0.5-4 h) but they have a wide range of bioavailability (from a low of 13% for eprosartan to a high of 60-80% for irbesartan); food does not influence the bioavailability, except for valsartan (a reduction of 40-50%) and eprosartan (increase). A limited dose-peak plasma levels/areas under the plasma level-time curve proportionality is observed for some of the ARBs. Most of these drugs have high plasma protein binding (95-100%); irbesartan has the lowest binding among the group (90%). The steady-state volumes of distribution vary from a low of 9 L (candesartan) to a high of 500 L (telmisartan). (ABSTRACT TRUNCATE