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Micardis (Telmisartan)

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

Other names for this medication:

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


Also known as:  Telmisartan.


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

Generic name of Micardis is Telmisartan.

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

Brand name of Micardis is Micardis.


Take Micardis orally, usually once a day.

You may take this drug with or without food.

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

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

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

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

Most people with high blood pressure do not feel sick.

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


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


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

Side effects

The most common side effects associated with Micardis are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


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

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

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

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

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

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

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

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

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

Avoid alcohol.

Avoid machine driving.

Do not stop taking Micardis suddenly.

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Middle-aged adults with type 2 diabetes but without severe albuminuria from the Ongoing Telmisartan Alone and in Combination With Ramipril Global Endpoint Trial (ONTARGET; n=6,916).

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The present study was designed to investigate the potential of telmisartan, an angiotensin AT(1) receptor, in chronic constriction injury-induced neuropathic pain in rats. Four loose ligatures were placed around the sciatic nerve to induce chronic constriction injury and neuropathic pain. Acetone drop, pin-prick, hot plate and paint brush tests were performed to assess cold allodynia; mechanical and heat hyperalgesia; and dynamic mechanical allodynia, respectively along with assessment of spontaneous pain and postural index in terms of foot deformity. The levels of TNF-α were measured in the sciatic nerve as an index of inflammation. Chronic constriction injury was associated with development of cold allodynia; mechanical and heat hyperalgesia; dynamic mechanical allodynia; and spontaneous pain and foot deformity along with rise in the levels of TNF-α. Telmisartan (1, 2, 5 mg/kg, p.o.) was administered for 14 days in chronic constriction injury subjected rats. Administration of telmisartan (2, 5 mg/kg) significantly attenuated chronic constriction injury-induced pain related behavior, foot deformity and rise in TNF-α level. It may be concluded that telmisartan has a potential in attenuating neuropathic pain behavior in chronic constriction injury model which may possibly be attributed to its anti-inflammatory properties.

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Male Wistar albino rats were randomly divided into five groups of 10 rats each: (i) non-ligated, given water; (ii) ligated, given water; (iii) ligated, given 1 mg/kg TELM; (iv) ligated, given 5 mg/kg TELM; and (v) ligated, given 10 mg/kg TELM. All groups were treated with saline or TELM for 10 days. Periodontal tissue was analysed by histopathology; by the immunohistochemical examination of COX-2, MMP-2, MMP-9 and the RANKL/RANK/OPG pathway; and by ELISA analysis of the levels of IL-1β, IL-10, TNF-α, myeloperoxidase (MPO), malonaldehyde (MDA) and glutathione (GSH).

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AT1 antagonism inhibited vessel wall inflammation and inhibition of PI3K/Akt may be involved in the modulation of the MCP-1/CCR2 system by AT1 antagonists in SHRs.

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CCN genes are activated in heart failure. Their regulation is multidimensional both transcriptional and posttranscriptional. The involved pathways include angiotensin II and IL-6.

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Hypertension is a major risk factor for cardiovascular disease, and data regarding the efficacy and tolerability of telmisartan compared with losartan on blood pressure (BP) control in patients with hypertension.

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In this study, the binding of hemoglobin (Hb) with three benzimidazole-biphenyl derivatives (telmisartan (TST), candesartan (CST), and DB921) is investigated by molecular docking, molecular dynamics (MD) simulation, and binding free energy calculation. Results demonstrate that the three drugs locate in the cavities formed by α1, α2, and β2 subunits. The average gyration radii are estimated and consistent with available experimental results. The binding free energies suggest that the binding site of CST/Hb is more stable than those of TST/Hb and DB921/Hb. The energy decomposition analysis is performed and reveals that the electrostatic interactions play an important role in the stabilization of the binding site of CST/Hb or DB921/Hb while the van der Waals interactions contribute largely to stabilization of the binding site of TST/Hb. The key residues stabilizing the binding sites of TST/Hb, CST/Hb, and DB921/Hb are identified based on the residue decomposition analysis. The probability densities of salt bridge distances demonstrate that there still exist the four salt bridges between α1 and α2 subunits of Hb in presence of these drugs.

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The effect of the AT1-receptor antagonists losartan, irbesartan, and telmisartan on angiotensin II (Ang II)-induced facilitation of noradrenergic neurotransmission was investigated in the isolated rat mesenteric artery under isometric conditions. Electrical field stimulation (2, 4, and 8 Hz) caused a frequency-dependent increase of contractile force. At stimulation frequencies of 2, 4, and 8 Hz, Ang 11 (10 nM) increased the stimulation-induced vasoconstrictor responses by a factor 4.8 +/- 0.9, 2.9 +/- 0.7, and 1.3 +/- 0.1, respectively (p < 0.05 compared with control for all frequencies). The enhancement could be concentration-dependently antagonized by losartan (1 nM-1 microM), irbesartan (0.1 nM-0.1 microM), and telmisartan (0.01 nM-0.01 microM). At a stimulation frequency of 2 Hz, the relation between stimulation-induced vasoconstrictor responses (in presence of Ang II 10 nM) and the concentration of the AT1-antagonists used could be described by linear regression. The order of potency concerning sympathoinhibition was telmisartan > irbesartan > losartan (p < 0.05 between linear regression lines). Contractile responses to exogenous noradrenaline were unaltered in the presence of Ang II 10 nM. We conclude that the facilitating effect of Ang II on noradrenergic neurotransmission is mediated by presynaptically located AT1-receptors. Conversely, this facilitating effect can be dose-dependently counteracted by blockade of these receptors. Sympathoinhibitory properties are likely to contribute to the therapeutic effect of AT1-blockers, in particular in conditions in which the sympathetic nervous system is activated, such as congestive heart failure and hypertension.

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A novel molecularly imprinted solid-phase extraction with spectrofluorimetry method has been developed for the selective extraction of telmisartan from human urine. Molecularly imprinted polymers were prepared by a noncovalent imprinting approach through UV-radical polymerization using telmisartan as a template molecule, 2-dimethylamino ethyl methacrylate as a functional monomer, ethylene glycol dimethacrylate as a cross-linker, N,N-azobisisobutyronitrile as an initiator, chloroform as a porogen. Molecularly imprinted polymers and nonimprinted control polymer sorbents were dry-packed into solid-phase extraction cartridges, and eluates from cartridges were analyzed using a spectrofluorimeter. Limit of detection and limit of quantitation values were 11.0 and 36.0 ng/mL, respectively. A very high imprinting factor (16.1) was achieved and recovery values for the telmisartan spiked in human urine were in the range of 76.1-79.1%. In addition, relatively low within-day (0.14-1.6%) and between-day (0.11-1.31%) precision values were obtained. Valsartan was used to evaluate the selectivity of sorbent as well. As a result, a sensitive, selective, and simple molecularly imprinted solid-phase extraction with spectrofluorimetry method has been developed and successfully applied to the direct determination telmisartan in human urine.

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To observe the effects of telmisartan on Kv1.3 and Kv1.5 potassium channels expressed in Xenopus oocytes.

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Post hoc observational analysis of a multicenter trial involving 20,330 patients (age ≥50 years) with recent non-cardioembolic ischemic stroke; patients were recruited from 695 centers in 35 countries from September 2003 through July 2006 and followed up for 2.5 years (follow-up ended on February 8, 2008). Patients were categorized based on their mean SBP level: very low-normal (<120 mm Hg), low-normal (120-<130 mm Hg), high-normal (130-<140 mm Hg), high (140-<150 mm Hg), and very high (≥150 mm Hg).

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Prolonged lowering of blood pressure after a stroke reduces the risk of recurrent stroke. In addition, inhibition of the renin-angiotensin system in high-risk patients reduces the rate of subsequent cardiovascular events, including stroke. However, the effect of lowering of blood pressure with a renin-angiotensin system inhibitor soon after a stroke has not been clearly established. We evaluated the effects of therapy with an angiotensin-receptor blocker, telmisartan, initiated early after a stroke.

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We tested the hypothesis that patients with ACE inhibitor-associated angioedema present during months when pollen counts are increased.

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The study included evaluation of respiratory function, bronchial conductivity, gas homeostasis, and 24-hour profile of blood pressure (BP) in 15 male patients with chronic obstructive lung disease and I-II stage arterial hypertension prior to and after 2 weeks of therapy with telmisartan. The drug, administered in a dose of 80 mg/day, significantly increased 1 sec forced expiratory volume, peak expiratory flow rate, decreased effective bronchial resistance and CO2 partial pressure in arterial blood. Telmisartan also significantly reduced mean systolic BP (SBP) (p < 0.003) and diastolic BP (DBP) (p < 0.001) during day hours, SBD (p < 0.01) and pulse BP (p < 0.05) during night hours, significantly reduced SBP load (p < 0.02) and DBP load (p < 0.003) during day hours, and SBP load during night hours (p < 0.02).

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Treatments with ACEI and ARBs reduced the incidence of the occurrence of cataract. The effect of combinational drugs of ACEI (ramipril) and AT1 receptor blocker (Telmisartan) was evaluated. The drugs used in combinations showed improvement in the histopathological and biochemical changes of the diabetic animals, both for the retina and kidney.

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A PubMed literature search was conducted to identify evidence on the use of telmisartan for preventing CV events.

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Telmisartan is an angiotensin II receptor blocker with peroxisome proliferator-activated receptor-gamma agonistic properties. Telmisartan prevents weight gain and decreases food intake in models of obesity and in glitazone-treated rodents. This study further investigates the influence of telmisartan and pioglitazone and their association on weight gain and body composition by examining their influence on neuroendocrine mediators involved in food intake. Male C57/Black 6 mice were fed a high-fat diet, weight matched, and randomized in 4 treatment groups: vehicle, pioglitazone, telmisartan, and pioglitazone-telmisartan. Weight gain, food and water intake, body composition, plasma leptin levels, and the hypothalamic expression of neuroendocrine mediators were analyzed. Additional studies were performed with irbesartan and in angiotensin II 1(A) receptor-knockout mice. Telmisartan abolished weight and fat gain in vehicle- and pioglitazone-treated mice while decreasing food intake, the hypothalamic expression of the agouti-related protein, and plasma leptin levels. Modifications in neuropeptide Y and proopiomelanocortin were not consistent with changes in food intake. The effects on weight gain and expression of the agouti-related protein were intermediate with irbesartan. The effects of telmisartan on weight gain were even more pronounced in angiotensin II 1(A) receptor-knockout mice. This study confirms the anorexigenic effects of telmisartan in mice fed a high-fat diet and suggests for the first time a functional role of telmisartan on hypothalamic orexigenic agouti-related protein regulation. These anorexigenic properties abolish both weight gain and body composition modifications in fat-fed and glitazone-treated mice. The anorexigenic properties are independent from the angiotensin II 1(A) receptor.

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Boehringer Ingelheim.

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The mean +/- SE fall in renal plasma flow (RPF) in response to intravenous N(G)-monomethyl-L-arginine (L-NMMA), reflecting the magnitude of nitric oxide (NO) activity, increased with telmisartan from 71.9 +/- 9.0 ml/min before therapy to 105.2 +/- 9.7 ml/min at the end of treatment (P < 0.001). With ramipril, RPF response to L-NMMA increased from 60.1 +/- 12.2 to 87.8 +/- 9.2 ml/min (P = 0.018). The adjusted difference between treatments was -17.1 +/- 13.7 ml/min (P = 0.214). In accordance, telmisartan increased RPF at rest (i.e., without L-NMMA) from 652.0 +/- 27.0 to 696.1 +/- 31.0 ml/min (P = 0.047), whereas ramipril produced no significant changes in RPF. The more the basal NO activity improved, the greater was the vasodilatory effect on renal vasculature (r = 0.47, P < 0.001).

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Male Sprague-Dawley rats were randomly divided into 3 groups: sham operation, abdominal aortic coarctation (AAC) and AAC + telmisartan. Telmisartan (5 mg · kg · d) or vehicle was infused into the stomach 1 week after the operation. ER stress signaling pathway molecules and apoptosis were studied in pressure-overloaded hearts 9 weeks after AAC.

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The CD feeding induced obesity, hyperphagia, hyperlipidaemia, and leptin and insulin resistance. Telmisartan reduced the CD-induced increase in body weight and abdominal fat mass. Whereas energy intake was higher rather than lower, the respiratory ratio was lower. After telmisartan, leptin-induced energy intake was reduced and respiratory ratio was increased compared with C(CD) rats. Telmisartan also decreased plasma levels of triglycerides, free fatty acids and low-density lipoprotein. Amlodipine alone or the combination telmisartan + amlodipine did not affect body weight and eating behaviour. Telmisartan, but not amlodipine and telmisartan + amlodipine, improved glucose utilization. The decrease in BP reduction was almost the same in all treatment groups.

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This study examined the effects of increasing the thiazide diuretic dose in a fixed-dose ARB/diuretic combination in patients with uncontrolled hypertension despite 6 weeks' open-label treatment with the ARB/diuretic combination, telmisartan 80 mg/hydrochlorothiazide 12.5 mg (T80/H12.5). 713 patients with trough seated DBP =90 mmHg were then randomized to 8 weeks' double-blind treatment with telmisartan 80 mg and an increased dose of 25 mg of hydrochlorothiazide (T80/H25) or T80/H12.5. Adjusted mean seated DBP changes from baselines of 95.3 (T80/H25) and 95.0 mmHg (T80/H12.5) were -7.1 and --5.5 mmHg (difference: 1.6 mm Hg), respectively (P=.0012). Changes in systolic blood pressure from 147.9 mmHg (T80/H25) and 147.4 mmHg (T80/H12.5) were -9.8 and -7.1 mmHg (difference: 2.7 mm Hg) (P=.0003). Adverse events occurred in 31.5% (T80/H25) and 29.6% (T80/H12.5), with serious events in 1.4% and 0.8%, respectively. Hypokalemia was rare. These results show that higher-dose thiazide diuretic in combination with T80 in patients with hypertension uncontrolled by T80/H12.5 provides additional blood pressure reductions and is well tolerated.

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The metabolic syndrome is associated with activation of the renin-angiotensin system. However, whether the coronary vascular response to ANG II is altered under this condition is unknown. Experiments were conducted in control and chronically high-fat-fed dogs with the prediabetic metabolic syndrome both in vitro (isolated coronary arterioles, 60-110 microm) and in vivo (anesthetized and conscious). We found that plasma renin activity and ANG II levels are elevated in high-fat-fed dogs and that this increase in ANG II is associated with a significant increase in ANG II-mediated coronary vasoconstriction in isolated coronary arterioles and in anesthetized open-chest dogs. The vasoconstriction to ANG II is abolished by ANG II type 1 (AT1) receptor blockade. In conscious chronically instrumented dogs, AT1 receptor blockade with telmisartan improved the balance between coronary blood flow and myocardial oxygen consumption in the high-fat-fed dogs but not in normal control dogs, i.e., the relationship between coronary venous Po2 and myocardial oxygen consumption was shifted upward, toward normal control values. Quantitative assessment of coronary arteriolar AT1 and ANG II type 2 (AT2) receptor mRNA levels by real-time PCR revealed no significant difference between normal control and high-fat-fed dogs; however, Western blot analysis showed a significant increase in AT1 receptor protein level with no change in AT2 receptor protein density. These findings indicate that AT1 receptor-mediated coronary constriction is augmented in the prediabetic metabolic syndrome and contributes to impaired control of coronary blood flow via increases in circulating ANG II and/or coronary arteriolar AT1 receptor density.

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The purpose of the present study was to evaluate the effect of Telmisartan (Tel) and Losartan (Los) on nanoparticle intratumoral distribution and anticancer effects in lung cancer. A549 lung tumor cells were orthotopically and metastatically administered to Nu/nu mice. Fluorescent polystyrene nanoparticles (FPNPs, size ~200 nm) beads were used to study their intratumoral distribution after Tel and Los treatments. Animals were administered with FPNPs and after 2h, FPNPs intratumoral distribution was studied by fluorescent microscopy. Tel (~1.12 mg/kg) and Los (~4.5mg/kg) were administered by inhalation delivery at alternative days for 4 weeks to tumor bearing animals. Collagen-1, transforming growth factor beta 1 (TGF-β1), cleaved caspase-3, Vimentin and E-Cadherin expressions were studied by western blotting. To correlate the AT1 receptor blockage to anticancer effects, VEGF levels and microvessel densities (MVD) were quantified. Los and Tel treated group resulted in the 5.33 and 14.33 fold increase respectively in the FPNPs intratumoral distribution as compared to the controls. Tel treatment attenuated 2.23 and 1.70 fold Collagen 1 expression compared to untreated control and Los groups, respectively. Further, in Tel and Los treated groups, the TGF-β1 active levels were significantly (p<0.05) decreased. Tel (at four times less dose) was 1.89 and 1.92 fold superior in anticancer activity to Los respectively in A549 orthotopic and metastatic tumor models (p<0.05) when given by inhalation route. Tel, by virtue of its dual pharmacophoric nature could be an ideal candidate for combination therapy to improve the nanoparticle intratumoral distribution and anticancer effects.

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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 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.

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micardis generic price 2016-03-15

Primary objectives of the ONgoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) are to determine if the combination of the ARB telmisartan and the ACE inhibitor ramipril is more effective than ramipril alone, and if telmisartan is at least as effective as ramipril. The Telmisartan Randomized AssessmeNt Study buy micardis online in aCE iNtolerant subjects with cardiovascular Disease (TRANSCEND) will determine if telmisartan is superior to placebo in patients who are intolerant of ACE inhibitors. The primary outcome for both trials is the composite of cardiovascular death, myocardial infarction, stroke, or hospitalization for heart failure.

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ONTARGET has established the efficacy of the angiotensin receptor blocker (ARB) telmisartan to slow disease progression and delay buy micardis online or prevent morbid events in patients with atherosclerosis. Although the study failed to confirm additive efficacy of telmisartan and the angiotensin-converting-enzyme (ACE) inhibitor ramipril, caution should be exercised in assuming that the mean response in a clinical trial applies to individual patients who might benefit from combination therapy. Physicians should also recognize that the design of the study, in which full doses of the ACE inhibitor and the ARB were administered, might not replicate clinical practice, where one drug is usually added to the other.

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Patients with type 2 diabetes are prone to hypertension and persistent protein leakage from the kidney (microalbuminuria or macroalbuminuria). A progressive decline in renal function can lead to overt diabetic nephropathy and ESRD. The likelihood of cardiovascular disease also is increased. Control of hypertension is paramount to prevent these life-threatening complications. Agents that target the renin-angiotensin system--angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers--have been shown to be renoprotective. The groundbreaking Diabetics Exposed to Telmisartan And enalaprIL (DETAIL) trial was designed to address the absence of comparative data on the long-term effects of an angiotensin II receptor blocker versus an angiotensin-converting enzyme inhibitor on renoprotection and buy micardis online survival in 250 patients with hypertension and early type 2 diabetic nephropathy. The primary purpose of the 5-yr double-blind, double-dummy, randomized study was to establish whether 40 to 80 mg of telmisartan conferred similar (i.e., noninferior) renoprotection to 10 to 20 mg of enalapril as determined by the change from baseline in GFR, measured by the plasma clearance of iohexol. Secondary end points included the emergence of ESRD and all-cause mortality. Telmisartan was not inferior to enalapril in reducing the decline in GFR: Mean annual declines in GFR were 3.7 and 3.3 ml/min per 1.73 m(2) with telmisartan and enalapril, respectively. During the 5-yr study period, no patient developed a serum creatinine >200 micromol/L, and none required dialysis. There were only six deaths in each treatment group during the study, with half being due to cardiovascular events.

micardis dose maximum 2015-12-24

To study antihypertensive efficacy of monotherapy with telmisartan and its action on left ventricular buy micardis online myocardium remodeling in patients with hypertension.

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The ever-increasing introduction of new therapeutic agents means that the potential for drug interactions is likely to escalate. Numerous different classes of drugs are currently used to treat hypertension. The angiotensin receptor blockers offer one of the newest approaches to the management of patients with high blood pressure. Compared with other classes of antihypertensive agents, the angiotensin receptor blockers appear overall to have a low potential for drug interactions, but variations within the class have been detected. Losartan and irbesartan have a greater affinity for cytochrome p450 (CYP) isoenzymes and, thus, are more likely to be implicated in drug interactions. There is pharmacokinetic evidence to suggest that such interactions could have a clinical impact. Candesartan cilexetil, valsartan and eprosartan have variable but generally modest affinity and telmisartan has no affinity for any of the CYP isoenzymes. In vitro studies and pharmacokinetic/pharmacodynamic evaluation can provide evidence for some interactions, but only a relatively small number of drug combinations are usually studied in this way. The absence of any pharmacokinetic evidence of drug interaction, however, should not lead to complacency. Patients should be made aware of possible interactions, especially involving the concurrent use of over buy micardis online -the-counter products, and it may be prudent for all patients receiving antihypertensive treatment to be monitored for possible drug interactions at their regular check-ups. The physician can help by prescribing agents with a low potential for interaction, such as angiotensin receptor blockers.

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Telmisartan is a highly lipid-soluble angiotensin receptor blocker (ARB), which improves insulin sensitivity and reduces triglyceride levels and, thus, is called metabo-sartan. We examined the effects of telmisartan on neurovascular unit (N-acetylglucosamine oligomer [NAGO], collagen IV, and glial fibrillary acidic protein [GFAP]) and neuroinflammation (matrix metalloproteinase-9 [MMP-9] and inflammasome) in brain of stroke-resistant spontaneously hypertensive rat (SHR-SR). At 12 weeks of age, SHR-SR received transient middle cerebral artery occlusion (tMCAO) for 90 minutes and were divided into the following 3 groups, that is, vehicle group, low-dose telmisartan group (.3 mg/kg/d), and high-dose telmisartan group (3 mg/kg/d, postoral). Immunohistologic analysis at ages 6, 12, and 18 months showed progressive decreases of NAGO-positive endothelium and collagen IV-positive basement membrane and progressive increases of MMP-9-positive neurons, GFAP-positive astrocytes, and NLRP3-positive inflammasome in the cerebral cortex of vehicle group. Low-dose telmisartan reduced such buy micardis online changes without lowering blood pressure (BP), and high-dose telmisartan further improved such changes with lowering BP. The present findings suggest that a persistent hypertension caused a long-lasting inflammation after tMCAO in SHR-SR, which accelerated neurovascular disruption and emergent inflammasome, and that telmisartan greatly reduced such inflammation and protected the neurovascular unit via its pleiotropic effects in living hypertensive rat brain after ischemic stroke.

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Angiotensin type 1 receptor blockers are widely used for the treatment of hypertension, and one angiotensin type 1 receptor blocker, telmisartan, specifically activates the peroxisome proliferator-activated receptor (PPAR)-gamma. We studied the impact of PPARgamma mutants on transcriptional control and interaction with cofactors to elucidate differences in the molecular mechanism between telmisartan and other PPARgamma agonists, thiazolidinediones (TZDs). We created several amino acid substitutions in the ligand binding domain of PPARgamma that, based on molecular modeling, may affect the binding of these agents. In transient expression experiments, wild-type PPARgamma-mediated transcription stimulated by telmisartan was more than one third of that stimulated by TZDs. The activation stimulated by TZDs was impaired, whereas activation stimulated by telmisartan was retained, in the H323Y, S342A, and H449A mutants. In the Y473A mutant, the TZD-induced activation was further impaired and lower than that of telmisartan-induced activation. Coexpression of coactivators enhanced the activation by both telmisartan and TZDs, but activation by telmisartan always exceeded that of TZDs in the Y473A mutant. Based on a mammalian two-hybrid assay, the interaction with corepressors was retained in Y473A. Telmisartan and TZDs, but not 9cis retinoic acid, dissociated corepressors from the wild-type PPARgamma. Telmisartan most effectively dissociated corepressors from Y473A. The interaction with coactivators was enhanced by TZD activation of wild-type PPARgamma and both telmisartan and TZD activation of Y473A. Thus, the Y473A mutant is selectively stimulated buy micardis online by telmisartan but not TZDs, suggesting that telmisartan and TZDs have differential effects on the transcriptional control. In conclusion, these PPARgamma mutants could be powerful tools for developing novel therapeutic agents that retain the metabolic efficacy of PPARgamma activation with fewer adverse effects, such as the increase in body weight associated with TZDs.

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The 90% confidence intervals for buy micardis online the test/reference ratio of the pharmacokinetic parameters in fasting state (mean Cmax, AUC0-t, and AUC0-∞) were within the acceptable range of 80.00-125.00. Thus, these findings clearly indicate that the FDC product is bioequivalent with the individual marketed products in terms of rate and extent of drug absorption and is well tolerated with no significant adverse reactions.

micardis drug class 2017-01-17

Monotherapy with an ACE inhibitor was associated with blood-pressure control in most patients with ADPKD and stage 3 chronic kidney disease. The addition buy micardis online of an ARB did not alter the decline in the estimated GFR. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and others; HALT-PKD [Study B] number, NCT01885559.).

micardis generic name 2017-12-03

Compared with the control cells, the cells positive for β-gal staining was significantly increased in the Ang II model group, and showed cell cycle arrest at G0/G1 phase with decreased S and G2/M phase cell percentage, eNOS expression and cell viability (P<0.05). The extracts and telmisartan treatment of Ang II-induced cells resulted in decreased β-gal positive cells with a reduction in G0/G1 phase cells and an increasing in S, G2/M phase cells and eNOS expression (P<0.05). At 24 h, the extracts were more effective than telmisartan ( buy micardis online P<0.05); while telmisartan was more effective at 48 h (P<0.05).

micardis generic 2015-12-23

It was demonstrated that candesartan cilexetil, irbesartan and telmisartan had the potential to inhibit the transport of various drugs via P-gp. Telmisartan, which buy micardis online caused an increase in the serum digoxin concentration in humans, had a sufficiently high [I]/IC(50) value, suggesting that DDI between digoxin and telmisartan was caused by the inhibition of digoxin efflux via intestinal P-gp.

micardis cost 2017-08-11

We enrolled 31,506 participants for whom complete information on atrial fibrillation was available, 70.4% of whom were men. The mean age of participants was 66.5 years, and the mean baseline MMSE score was 27.7 (standard deviation 2.9) points. At baseline, 1016 participants (3.3%) had atrial fibrillation, with the condition developing in an additional 2052 participants (6.5%) during buy micardis online a median follow-up of 56 months. Atrial fibrillation was associated with an increased risk of cognitive decline (hazard ratio [HR] 1.14, 95% confidence interval [CI] 1.03-1.26), new dementia (HR 1.30, 95% CI 1.14-1.49), loss of independence in performing activities of daily living (HR 1.35, 95% CI 1.19-1.54) and admission to long-term care facilities (HR 1.53, 95% CI 1.31-1.79). Results were consistent among participants with and without stroke or receiving antihypertensive drugs.

dosage micardis plus 2015-09-07

Among these Indian patients with stage II hypertension, the FDC of T+A was found to be significantly buy micardis online more effective, with regard to BP reductions, than A, and both treatments were well tolerated.

micardis hct reviews 2017-12-27

Telmisartan was the study drug in 30,014 (85.7%) patients who received ARBs as part of the trials with new cancer data. Patients randomly assigned to receive ARBs had a significantly increased risk of new cancer occurrence compared with patients in control groups (7.2%vs 6.0%, risk ratio [RR] 1.08, 95% CI 1.01-1.15; p=0.016). When analysis was limited to trials where cancer was a prespecified endpoint, the RR was 1.11 (95% CI 1.04-1.18, p=0.001). Among specific solid organ cancers examined, only new lung-cancer occurrence was significantly higher in patients randomly assigned to receive ARBs than in those assigned to receive control (0.9%vs 0.7%, RR 1.25, 1. buy micardis online 05-1.49; p=0.01). No statistically significant difference in cancer deaths was observed (1.8%vs 1.6%, RR 1.07, 0.97-1.18; p=0.183).

micardis 60 mg 2015-10-30

The SH rats received a single oral dose of 2, 4, and 8 mg/kg of telmisartan. The plasma concentrations of telmisartan were determined by the liquid chromatography-mass spectrum method. The mean arterial blood pressure was measured to characterize the pharmacodynamics of telmisartan by tail-cuff manometry. The relationship for the telmisartan concentration-hypotensive effect in the Biaxin Dosing SH rats was characterized using an indirect response model.

micardis and alcohol 2017-10-12

Both ramipril and telmisartan improve echocardiographic left ventricular diastolic indices and reduce Imitrex Buy plasma BNP levels in diabetic patients; their combination yields an even better therapeutic effect.

micardis dosage maximum 2017-05-12

Hypertension and insulin resistance are associated with reduced coronary vasodilatory capacity, possibly caused by structural changes in the coronary resistance vessels. The goal of this study was to compare the effect of an angiotensin receptor blocker (ARB) with that of a calcium channel blocker (CCB) on coronary flow reserve and insulin Anafranil 600 Mg resistance among essential hypertensive patients without left ventricular hypertrophy. A total of 40 consecutive essential hypertensive patients were randomized to daily 40 mg telmisartan or 20 mg nifedipine coat-core treatment. Coronary flow velocity reserve (CFVR) measurement using transthoracic Doppler echocardiography and blood tests were performed before and after 12 weeks of treatment. At baseline, blood pressure, CFVR, and homeostasis model assessment of insulin resistance (HOMA-IR) were not significantly different between the two groups. At the end of the treatment period, the telmisartan and nifedipine groups exhibited similar declines in blood pressure. CFVR was improved in the telmisartan group (2.4+/-0.4 to 2.9+/-0.4; p<0.01), but there was no difference in the nifedipine group (2.5+/-0.3 to 2.5+/-0.3; n.s.). HOMA-IR was improved in the telmisartan group (3.1+/-1.1 to 1.6+/-0.7; p<0.01), but there was no difference in the nifedipine group (2.8+/-1.1 to 2.4+/-0.7; n.s.). In conclusion, this study demonstrates that antihypertensive therapy with telmisartan, but not nifedipine, has a beneficial effect on coronary microcirculation and insulin resistance among essential hypertensive patients.

micardis maximum dose 2016-11-24

A 66 year-old woman with no history of renal or liver disease presented with progressive asthenia and diffuse myalgia. She cited 5 months history of mild hyperlipidemia under treatment with rosuvastatin (10 mg/day). Clinical examination documented both an increase in liver size and proximal muscle weakness, with difficulty in raising arms above the head. Blood tests showed the presence of renal, liver and muscle failure, with no evidence of virological, immunological or haematological diseases. Rosuvastatin treatment was stopped and blood values normalised within five days; but because of an increase in cholesterol plasma levels, rosuvastatin (10 mg/day) was restarted. Two days later, the patient returned to our observation due to the Valtrex Drug Interactions development of asthenia and muscle weakness, with an increase in creatine phosphokinase, 12,165 U/l. Rosuvastatin was discontinued and replaced with pravastatin (40 mg/day) with a complete resolution of clinical and laboratory findings in about six days. Our patient was taking rosuvastatin, warfarin and telmisartan, which are metabolised by CYP2C9; we therefore hypothesised that the rosuvastatin-induced rhabdomyolysis was probably by CYP2C9 enzyme saturation.

micardis generic release 2015-01-13

Telmisartan therapy reduced NOS activity and/or expression in these subjects, possibly because of improved vascular function arising from AT(1) Rulide Drug receptor blockade.

micardis dosage instructions 2017-03-15

The mechanism by which drugs inhibit organic anion transporter 1 (OAT1) was examined. OAT1 was stably expressed in Chinese hamster ovary (CHO) cells, and para-aminohippurate (PAH) and 6-carboxyfluorescein were the substrates. Most compounds (10 of 14) inhibited competitively, increasing the Michaelis constant (Km) without affecting the maximal transport rate (Jmax). Others were mixed-type (lowering Jmax and increasing Km) or noncompetitive (lowering Jmax only) inhibitors. The Mobic The Drug interaction of a noncompetitive inhibitor (telmisartan) with OAT1 was examined further. Binding of telmisartan to OAT1 was observed, but translocation was not. Telmisartan did not alter the plasma membrane expression of OAT1, indicating that it lowers Jmax by reducing the turnover number. PAH transport after telmisartan treatment and its washout recovered faster in the presence of 10% fetal bovine serum in the washout buffer, indicating that binding of telmisartan to OAT1 and its inhibitory effect are reversible. Together, these data suggest that telmisartan binds reversibly to a site distinct from substrate and stabilizes the transporter in a conformation unfavorable for translocation. In the absence of an exchangeable extracellular substrate, PAH efflux from CHO-OAT1 cells was relatively rapid. Telmisartan slowed PAH efflux, suggesting that some transporter-mediated efflux occurs independent of exchange. Although drug-drug interaction predictions at OAT1 assume competitive inhibition, these data show that OAT1 can be inhibited by other mechanisms, which could influence the accuracy of drug-drug interaction predictions at the transporter. Telmisartan was useful for examining how a noncompetitive inhibitor can alter OAT1 transport activity and for uncovering a transport mode independent of exchange.

micardis generic launch 2016-01-17

The metabolic syndrome (MS) is a common risk factor for cardiovascular disease and type-2 diabetes. Recently, telmisartan, an angiotensin II receptor antagonist that has an antihypertensive effect, has been reported to be a partial peroxisome proliferator-activated receptor gamma (PPARgamma) agonist. The anti-diabetic hormone adiponectin has been recognized as a marker of in vivo PPARgamma activation. Therefore, we studied telmisartan's effect on the metabolic profile and adiponectin levels in a fructose-induced hypertensive, hyperinsulinemic, hyperlipidemic rat model. Twenty-four male Sprague-Dawley rats were divided into three groups (eight in each). One group of control rats was fed standard chow for 5 weeks while a second was fed a fructose-enriched diet. A third group was fed a fructose-enriched diet for 5 weeks Noroxin 200 Mg and treated with telmisartan 5 mg/kg/day during the last 2 weeks. Fructose feeding increased systolic blood pressure (mean+/-SEM), from 130+/-1 to 148+/-2 mmHg, insulin from 0.26+/-0.03 to 0.68+/-0.08 ng/mL, and triglycerides from 102+/-6 to 285+/-23 mg/dL (p<0.05 for all variables). Telmisartan treatment reversed these effects and reduced blood pressure to 125+/-2 mmHg, insulin levels to 0.41+/-0.07 ng/mL, and triglycerides to 146+/-18 mg/dL (p<0.05 for all variables), while attenuating the increase in body weight during weeks 3 to 5. In contrast, telmisartan did not affect plasma adiponectin levels. In conclusion, although telmisartan is considered a partial PPARgamma agonist, its beneficial effect in the fructose-induced hypertension, hypertriglyceridemia, and hyperinsulinemia rat model is apparently not mediated by adiponectin elevation but rather by direct inhibition of AT1 receptor.

micardis generic cost 2017-02-21

Although angiotensin II (Ang II) binds to Ang II type 1 (AT(1)) and type 2 (AT(2)) receptors, AT(1) and AT(2) receptors have antagonistic actions with regard to cell signaling. The molecular mechanisms that underlie this antagonism are not well understood. We examined AT(1) and AT(2) receptor-induced signal cross-talk in the cytoplasm and the importance of the hetero-dimerization of AT(1) receptor with AT(2) receptor on the cell surface. AT(1) and AT(2) receptors showed antagonistic effects toward inositol phosphate production. AT(1) receptors mainly formed homo-dimers, rather than hetero-dimers with AT(2) receptor, on the cell surface as determined by immunoprecipitation, and subsequently induced cell signals. AT(2) receptor mainly formed homo-dimers, rather than hetero-dimers with AT(1) receptor, on the cell surface. The expression levels of homo-dimerized AT(1) receptor or AT(2) receptor on the cell surface did not change after treatment with Ang II, the AT(1) receptor antagonist telmisartan or the AT(2) receptor antagonist PD123319. Finally, AT(1) and AT(2) receptor-induced signals antagonized phospholipase C-beta(3) phosphorylation. In conclusion, Ang II-induced AT(1) receptor signals may be mainly blocked by AT(2) receptor signals through their negative cross-talk in the cytoplasm rather than by the hetero-dimerization of both receptors on the cell surface. The proper balance of the expression levels of AT(1) and AT(2) receptors might be critical for the antagonistic action between these receptors.

micardis overdose death 2016-01-04

Individuals with transient ischemic attack and ischemic stroke have a high risk of recurrent stroke and death. While acetylsalicylic acid (ASA, aspirin) is proven and accepted as standard therapy in these patients, recent trials demonstrate that a combination of ASA and dipyridamole (DP) or clopidogrel may be superior to ASA. Blocking the renin-angiotensin system with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may also reduce recurrent stroke. The ongoing PRoFESS (Prevention Regimen for Effectively Avoiding Second Strokes) trial is designed to evaluate whether ASA + extended-release DP compared to clopidogrel, and whether telmisartan in addition to usual care in individuals after a stroke, will reduce the risk of further strokes.

micardis 20 mg 2015-02-15

Knowledge of glomerular structural and hemodynamic changes in vivo is still limited under diabetic conditions. In this study, we examined the alterations in glomerular structure and permeability of macromolecules and the effects of telmisartan using a confocal laser microscope.

micardis 80 mg 2016-11-03

Because growing evidence suggests that angiotensin II receptor blockers (ARBs) effectively inhibit oxidative stress, amyloid beta protein (Aβ) metabolism, and tau phosphorylation in animal brains, ARBs are considered to be a potential candidate for the treatment of Alzheimer's disease (AD). Consistent with such basic studies, two recent observational studies and a small prospective, randomized, open-label trial have shown the effectiveness of ARBs in preventing AD and/or slowing its progression. Nonetheless, large clinical trials have not shown their effectiveness, but their results are debatable because of short follow-up durations and heterogeneity of the cognition assessments used in the studies. Because a recent analysis of the Honolulu-Asia Aging study showed that abnormalities of the serum Aβ level begin approximately 15 years before the diagnosis of AD, long-term clinical trials assessing dementia as a primary endpoint with sensitive measurements of cognition and brain imaging techniques will clarify the effectiveness of ARBs in AD treatment.

micardis patient reviews 2016-03-16

These data demonstrated that application of a renin-angiotensin system blocker plus a vitamin D analog effectively prevented renal injury in ADR-induced nephropathy. The observed amelioration of renal injury may be partly attributable to antiapoptotic effects in podocytes.

micardis 120 mg 2016-02-13

60 adults with Stages 2 - 3 CKD who had been receiving high-dose ARBs and had not achieved their target blood pressure of 130/80 mmHg were switched to a combination of telmisartan (40 mg) and HCTZ (12.5 mg) once daily for a 12-week study period. We measured the blood pressure, pulse rate, urinary protein excretion, and total monthly drug costs before and after the switch.

micardis dosage 2016-11-24

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

micardis overdose 2016-12-07

Telmisartan and pyridoxamine could attenuate abdominal aorta vascular remodeling via reducing oxidative stress and AGEs production as well as restoring the balance of VSMCs proliferation and apoptosis in SHRs abdominal aorta.

micardis hct dosage 2015-04-27

We sought to investigate the effects of telmisartan on high-fat diet-induced hypertension and to explore the possible underlying mechanisms. Rats receiving high-fat diet were randomly divided into two groups, the telmisartan group (n = 9) and the high-fat diet group (n = 10). The control group consisted of age-matched rats on a regular diet (n = 10). At the end of the treatment, the body weight, blood pressure, insulin sensitivity and serum adiponectin levels of all rats were examined, and their visceral fat was extracted and weighed. Our results showed that telmisartan improved insulin resistance and dyslipidemia and increased serum adiponectin levels. Telmisartan also lowered both systolic blood pressure and diastolic blood pressure, and decreased the accumulation of perirenal fat associated with high-fat diet. Furthermore, telmisartan increased adiponectin mRNA expression in the perirenal fat. Correlation analysis showed that both systolic blood pressure and diastolic blood pressure were positively correlated with perirenal fat. These effects of telmisartan may be mediated through decreases in perirenal fat and contributed to the improvement of perirenal fat function. Our findings suggested a strong link between perirenal fat and high-fat diet-induced hypertension, and identified telmisartan as a potential drug for the treatment of obesity-related hypertension.