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Benicar (Olmesartan)

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Benicar is used for treating high blood pressure, alone or with other medicines. It may also be used for other conditions.

Other names for this medication:

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Lasix, Norvasc, Toprol, Hyzaar, Teveten, Edarbi, Cozaar, Atacand, Micardis


Also known as:  Olmesartan.


Benicar is an angiotensin II receptor antagonist. It works by inhibiting the action of a chemical transmitter (angiotensin II) and allowing the blood vessels to dilate (widen) and the kidneys to eliminate extra sodium and fluids. These actions combine to help lower blood pressure.

Generic name of Benicar is Olmesartan.

Benicar is also known as Olmesartan, Olmetec, Olmezest, Olmecip.

Brand name of Benicar is Benicar.


Take Benicar orally with or without food.

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


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


Store your medicine at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children and in a container that small children cannot open.

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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 Benicar if you are allergic to Benicar components.

Do not take Benicar if you're pregnant or you plan to have a baby, or you are a nursing mother.

Avoid alcohol.

Avoid machine driving.

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

Be careful if you use salt substitute or a product that has potassium in it.

Do not stop taking Benicar suddenly.

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Participants received dual-combination treatment for 4 weeks or placebo for 2 weeks. Participants receiving placebo switched to dual-combination treatment from week 2 to week 4. At week 4, participants switched to triple-combination treatment or continued on dual-combination treatment until week 12.

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Chronic inhibition of nitric oxide (NO) synthesis by Nomega-nitro-L-arginine methyl ester (L-NAME) increases vascular tissue angiotensin II activity and oxidative stress in animals by incompletely understood mechanisms. In a rat model, we investigated the role of local angiotensin II activity in the pathogenesis of increased oxidative stress.

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Olmesartan medoxomil is an angiotensin II receptor antagonist. In pooled analyses of seven randomized, double-blind trials, 8 weeks' treatment with olmesartan medoxomil was significantly more effective than placebo in terms of the response rate, proportion of patients achieving target blood pressure (BP) and mean change from baseline in diastolic (DBP) and systolic blood pressure (SBP). Olmesartan medoxomil had a fast onset of action, with significant between-group differences evident from 2 weeks onwards. The drug was well tolerated with a similar adverse event profile to placebo. In patients with type 2 diabetes, olmesartan medoxomil reduced renal vascular resistance, increased renal perfusion, and reduced oxidative stress. In several large, randomized, double-blind trials, olmesartan medoxomil 20 mg has been shown to be significantly more effective, in terms of primary endpoints, than recommended doses of losartan, valsartan, irbesartan, or candesartan cilexetil, and to provide better 24 h BP protection. Olmesartan medoxomil was at least as effective as amlodipine, felodipine and atenolol, and significantly more effective than captopril. The efficacy of olmesartan medoxomil in reducing cardiovascular risk beyond BP reduction is currently being investigated in trials involving patients at high risk due to atherosclerosis or type 2 diabetes.

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To evaluate the safety and tolerability of a titrate-to-goal, olmesartan medoxomil-based therapy in patients with stage 1 hypertension (seated systolic BP [SeSBP] of 140-159 mmHg or seated diastolic BP [SeDBP] of 90-99 mmHg).

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Angiotensin II plays an important role in cardiac hypertrophy or remodeling. Angiotensin II receptor blockers (ARB) are clinically useful for the treatment of hypertension and heart failure. However, the molecular effects of ARB in the mechanically-stressed myocardium have not been completely defined. We investigated the effects of ARB on mechanically-modulated genes in cardiac myocytes.

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The objective of the present study was to analyze the cost-effectiveness of lifetime antihypertensive therapy with angiotensin II receptor blocker (ARB) monotherapy, calcium channel blocker (CCB) monotherapy, or ARB plus CCB (ARB+CCB) combination therapy in Japan. Based on the results of large-scale clinical trials and epidemiological data, we constructed a Markov model for patients with essential hypertension. Our Markov model comprised coronary heart disease (CHD), stroke, and progression of diabetic nephropathy submodels. Based on this model, analysis of the prognosis of each patient was repeatedly conducted by Monte Carlo simulation. The three treatment strategies were compared in hypothetical 55-year-old patients with systolic blood pressure (SBP) of 160 mmHg in the absence and presence of comorbid diabetes. Olmesartan medoxomil 20 mg/d was the ARB and azelnidipine 16 mg/d the CCB in our model. On-treatment SBP was assumed to be 125, 140, and 140 mmHg in the ARB+CCB, ARB alone, and CCB alone groups, respectively. Costs and quality-adjusted life years (QALYs) were discounted by 3%/year. The ARB+CCB group was the most cost-effective both in male and female patients with or without diabetes. In conclusion, ARB plus CCB combination therapy may be a more cost-effective lifetime antihypertensive strategy than monotherapy with either agent alone.

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317 clinical sites in the USA and Puerto Rico were included in the study.

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In a subgroup analysis based upon age, sex and race in patients aged ≥65 years with hypertension, an OM/HCTZ-based algorithm was efficacious and well tolerated. Identifier: NCT00412932.

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Cardiovascular disease is a major cause of premature death and disability worldwide, and effective blood pressure (BP) control is crucial for the reduction of cardiovascular risk in patients with hypertension. Despite this, many will fail to attain recommended BP goals. A reappraisal of European guidelines led to revised recommendations for BP reduction to values within the SBP/DBP range of 130 - 139/80 - 85 mmHg in all patients with hypertension, including higher-risk groups such as those with diabetes.

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Morin showed the highest Peff value 13.8 ± 0.34 × 10(-6 )cm/s in jejunum than ileum (p < .01) at 100 µM with absorption enhancement of 1.31-fold together with enhanced (p < .01) secretory transport of 6.27 ± 0.27 × 10 (-6 )cm/s in Caco-2 monolayer cells. Our findings noticed 2.37 (in-situ); 2.39 (in-vivo) and 1.43 (in-situ); 1.36 (in-vivo) fold increase in AUC0-t with elevated Cmax and shortened Tmax for freeze-dried solid dispersion in the presence of morin as compared to pure OLM and freeze-dried solid dispersions without morin, respectively.

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The primary endpoint was formulated before data collection began. It was the change in mean diastolic BP (DBP) from baseline to Week 10 in groups with HCTZ added to OLM/AML, compared with the corresponding dual OLM/AML therapy.

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This study demonstrated that the test and reference products met the regulatory criteria assuming bioequivalence. Both formulations were safe and well tolerated, and there were no noteworthy differences in the safety profiles of the test and reference drugs.

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In most patients with hypertension, especially Stage 2 hypertension, adequate control of blood pressure (BP) is only achieved with combination drug therapy. When using combination therapy, antihypertensive agents with complementary mechanisms of action are recommended, for example, an angiotensin receptor blocker (ARB) in combination with hydrochlorothiazide (HCTZ), a beta-blocker + HCTZ, an ACE inhibitor + HCTZ, or a calcium channel blocker + an ACE inhibitor. One such combination is olmesartan medoxomil + HCTZ, which is available as fixed-dose, single-tablet combinations for once-daily administration. In clinical trials, olmesartan medoxomil/HCTZ reduced systolic BP (SBP) and diastolic BP (DBP) to a greater extent than either component as monotherapy. A clinical study in patients with Stage 1 or 2 hypertension showed that olmesartan medoxomil/HCTZ achieved a similar mean reduction in DBP, but a significantly greater mean reduction in SBP and higher rate of BP control (< 140/90 mmHg) than observed with losartan/HCTZ, at US/European-approved starting doses. In a non-inferiority trial, the antihypertensive efficacy of olmesartan medoxomil/HCTZ was comparable to that of atenolol/HCTZ. Furthermore, indirect comparisons have shown that olmesartan medoxomil/HCTZ compares favorably with other antihypertensive combination therapies, including other ARB/HCTZ combinations and amlodipine besylate/ benazepril. Olmesartan medoxomil/HCTZ is generally well tolerated. In conclusion, olmesartan medoxomil/HCTZ is an effective and well-tolerated combination antihypertensive therapy that results in significant BP reductions and BP control in many patients.

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Retrospective analysis of data from 12 phase I-III trials in the US, Europe and Japan.

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Hypertension is a growing global health problem, and is predicted to affect 1.56 billion people by 2025. Treatment remains suboptimal, with control of blood pressure achieved in only 20%-35% of patients, and the majority requiring two or more antihypertensive drugs to achieve recommended blood pressure goals. To improve blood pressure control, the European hypertension guidelines recommend that angiotensin II receptor blockers (ARBs) or angiotensin-converting enzyme inhibitors (ACEIs) are combined with calcium channel blockers (CCBs) and/or thiazide diuretics. The rationale for this strategy is based, in part, on their different effects on the renin-angiotensin system, which improves antihypertensive efficacy. Data from a large number of trials support the efficacy of ACEIs or ARBs in combination with CCBs and/or hydrochlorothiazide (HCTZ). Combining two different classes of antihypertensive drugs has an additive effect on lowering of blood pressure, and does not increase adverse events, with the ARBs showing a tolerability advantage over the ACEIs. Among the different ARBs, olmesartan medoxomil is available as a dual fixed-dose combination with either amlodipine or HCTZ, and the increased blood pressure-lowering efficacy of these two combinations is proven. Triple therapy is required in 15%-20% of treated uncontrolled hypertensive patients, with a renin-angiotensin system blocker, CCB, and thiazide diuretic considered to be a rational combination according to the European guidelines. Olmesartan, amlodipine, and HCTZ are available as a triple fixed-dose combination, and significant blood pressure reductions have been observed with this regimen compared with the possible dual combinations. The availability of these fixed-dose combinations should lead to improvement in blood pressure control and aid compliance with long-term therapy, optimizing the management of this chronic condition.

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The majority of patients with hypertension, and in particular high-risk patients or those with diabetes mellitus or renal dysfunction, are likely to require combination therapy with at least two antihypertensive agents (from different classes) to achieve their blood pressure (BP) target. The delapril/manidipine fixed-dose combination consists of two antihypertensive agents with different, yet complementary, mechanisms of action. Delapril/manidipine has demonstrated short- and long-term antihypertensive efficacy in a number of clinical studies in patients with hypertension with an inadequate response to monotherapy. Comparative studies have demonstrated that delapril/manidipine is as effective as enalapril/hydrochlorothiazide (HCTZ) in patients with hypertension with an inadequate response to monotherapy, and as effective as irbesartan/HCTZ, losartan/HCTZ, olmesartan medoxomil/HCTZ, ramipril/HCTZ and valsartan/HCTZ in reducing BP in patients with hypertension and diabetes, or in obese patients with hypertension. Therapy with delapril/manidipine also appears to exert beneficial effects that extend beyond a reduction in BP, including nephroprotective activity and an improvement in fibrinolytic balance, supporting its value as a treatment option in these patient populations at high or very high cardiovascular risk because of the presence of organ damage, diabetes or renal disease.

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At week 12, OM 40/AML 10/HCTZ 25 mg resulted in significantly greater SeBP reductions in participants with diabetes (-37.9/22.0 mm Hg vs -28.0/17.6 mm Hg for OM 40/AML 10 mg, -26.4/14.7 mm Hg for OM 40/HCTZ 25 mg, and -27.6/14.8 mm Hg for AML 10/HCTZ 25 mg), CKD (-44.3/25.5 mm Hg vs -39.5/23.8 mm Hg for OM 40/AML 10 mg, -25.3/17.0 mm Hg for OM 40/HCTZ 25 mg, and -33.4/20.6 mm Hg for AML 10/HCTZ 25 mg), and chronic CVD (-37.8/20.6 mm Hg vs -31.7/18.2 mm Hg for OM 40/AML 10 mg, -30.9/17.1 mm Hg for OM 40/HCTZ 25 mg, and -27.5/16.1 mm Hg for AML 10/HCTZ 25 mg) (P<0.05 for all subgroups vs dual-component treatments). BP goal achievement was greater for participants receiving triple-combination treatment compared with the dual-combination treatments, and was achieved in 41.1%, 55.0%, and 38.9% of participants with diabetes, CKD, and chronic CVD on OM 40/AML 10/HCTZ 25 mg, respectively. At week 52, there was sustained BP lowering with the OM/AML/HCTZ regimen. Overall, the triple combination was well tolerated.

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As of February 26, 2007, this is the first published reported case of olmesartan medoxomil-induced angioedema. Practitioners should be aware of this rare but potentially serious adverse event.

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Hypertension is a known risk factor for cardiovascular events and mortality. The risk of cardiovascular events increases with age and is linear above 115/75 mm Hg. It also doubles for every 20/10-mm Hg elevation beyond this level and at every age level. Although guidelines vary somewhat by country, the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends a blood pressure (BP) goal of < 140/90 mm Hg for patients with uncomplicated hypertension and < 130/80 mm Hg for patients with type 2 diabetes mellitus (T2DM) or renal disease. Based on clinical evidence, patients with stage 1 hypertension (seated cuff systolic BP of 140-159 mm Hg or diastolic BP of 90-99 mm Hg) should be treated to targeted BP levels to reduce cardiovascular morbidity and mortality. The angiotensin II receptor blockers (ARBs) are well tolerated and demonstrate significant BP reduction. Olmesartan medoxomil (OM), an ARB, has been well studied and achieves significant BP lowering and goal achievement with good tolerability. Moreover, combination therapy comprising OM plus hydrochlorothiazide can significantly increase BP goal achievement without significantly increasing adverse events. This review evaluates clinical efficacy and safety data from 5 OM-based studies: 4 dose-titration studies and 1 factorial study. Study results demonstrate that OM ± hydrochlorothiazide is highly effective in reducing BP while enabling a majority of patients with stage 1 hypertension to achieve BP goal. In addition, OM tolerability data showed that the high achievement of BP goals was not attained at the expense of increased adverse events. This treatment is associated with low discontinuation rates, even in elderly patients and individuals with T2DM. The clinical data presented in this review support OM-based therapy as a rational and safe therapeutic option for patients with stage 1 hypertension.

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Olmesartan medoxomil (OM) is a prodrug-type angiotensin II type 1 receptor blocker (ARB). We recently identified carboxymethylenebutenolidase homolog (CMBL) as the responsible enzyme for OM bioactivation in humans. In the present study, we compared the bioactivating properties of OM with those of other prodrug-type ARBs, candesartan cilexetil (CC) and azilsartan medoxomil (AM), by focusing on interspecies differences and tissue specificity. In in-vitro experiments with pooled tissue subcellular fractions of mice, rats, monkeys, dogs, and humans, substantial OM-hydrolase activities were observed in cytosols of the liver, intestine, and kidney in all the species tested except for dog intestine, which showed negligible activity, whereas lung cytosols showed relatively low activities compared with the other tissues. AM-hydrolase activities were well correlated with the OM-hydrolase activities. In contrast, liver microsomes exhibited the highest CC-hydrolase activity among various tissue subcellular fractions in all the species tested. As a result of Western blot analysis with the tissue subcellular fractions, the band intensities stained with anti-human CMBL and carboxylesterase 1 (CES1) antibodies well reflected OM- and AM-hydrolase activities and CC-hydrolase activity, respectively, in animals and humans. Recombinant human CMBL and CES1 showed significant AM- and CC-hydrolase activities, respectively, whereas CC hydrolysis was hardly catalyzed with recombinant carboxylesterase 2 (CES2). In conclusion, OM is bioactivated mainly via intestinal and additionally hepatic CMBL not only in humans but also in mice, rats, and monkeys, while CC is bioactivated via hepatic CES1 rather than intestinal enzymes, including CES2. AM is a substrate for CMBL.

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Hyperinsulinemia and insulin resistance are associated with left ventricular hypertrophy (LVH) and cardiovascular complications in hypertensive subjects. The aim of this study was to explore the mechanisms for LVH including activation of the renin-angiotensin system system (RAS) and the sympathetic nervous system and their activation by insulin using a rat model of hyperinsulinemia and insulin resistance.

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Spinal cord injury is a major complication of thoracoabdominal aortic operations. We aimed to investigate neuroprotective role of olmesartan administered to rats before ischemia against ischemia-reperfusion (I-R) injury.

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Olmesartan-associated enteropathy (OAE) is characterised by diarrhoea, nausea, vomiting, abdominal pain, weight loss and severe sprue-like enteropathy, all of which are resolved after discontinuation of olmesartan medoximil.

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Following a 2-week placebo run-in, eligible patients were randomly assigned to receive olmesartan medoxomil 20mg (n = 319) or candesartan cilexetil 8mg (n = 324) once daily for 8 weeks.

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On the primary endpoint [reduction in mean sitting systolic blood pressure (SBP) after 12 weeks of treatment], the two treatments were similar (olmesartan medoxomil, -30.0 mmHg; nitrendipine, -31.4 mmHg). No significant difference between the treatment groups was observed, and non-inferiority of olmesartan medoxomil to nitrendipine was demonstrated using an analysis of covariance (ANCOVA) model. Reductions in mean sitting and standing SBP and diastolic blood pressure (DBP) up to week 24 were also similar with both treatments. Blood pressure (BP) goal attainment rates (sitting SBP

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In these adult patients with moderate to severe hypertension, triple combination treatment with OM 40 mg + AML 10 mg + HCTZ 25 mg was associated with significant BP reductions compared with dual combinations of the individual components. All treatments were generally well tolerated. ClinicalTrials. gov identifier: NCT00649389.

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Although the use of antihypertensive combination therapy has increased substantially in US adults over the last 20 years, such therapy remains considerably underutilized. Numerous studies have shown that combination therapies, including FDCs, can markedly reduce BP and adverse events relative to monotherapies, and this paper overviews data for various combination therapies: angiotensin-receptor blocker (ARB) + diuretic; angiotensin-converting enzyme (ACE) inhibitor + diuretic; calcium-channel blocker (CCB) + ACE inhibitor; and CCB + ARB. Specifically, fixed-dose CCB/ARB combinations of amlodipine with losartan, valsartan, or olmesartan medoxomil have recently been developed, and combination therapy schedules of amlodipine plus one of these ARBs have shown greater BP-lowering efficacy compared with the constituent monotherapies. Furthermore, in two large studies in a total of >3000 patients, CCB + ARB combination therapy was associated with significantly lower incidences of headache and peripheral edema than CCB monotherapy.

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A beneficial effect on glucose metabolism is reported with angiotensin receptor blocker (ARB) treatment of hypertension. The effect on blood glucose level during the course of treatment with ARBs in clinical cases is uncertain. Our objectives were to survey the changes in glucose and HbA1c levels in patients with hypertension over a one-year period, and to study the correlations between these values and the time after the start of ARB therapy.

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SeSBP reductions >50 mmHg were seen in 24.4% of participants receiving triple-combination treatment versus 8.1%-15.8% receiving dual-combination treatment. More participants receiving triple-combination treatment achieved the SeSBP target of <140 mmHg (73.6% versus 51.3%-58.8%; P < 0.001) and the seated blood pressure target of <140/90 mmHg (69.9% versus 41.1%-53.4%; P < 0.001). Prevalence and severity of adverse events were similar in all treatment groups.

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This study was designed to determine whether genetic polymorphisms of multidrug-resistant protein 2 (ABCC2), organic anion transporting polypeptide 1B1 (SLCO1B1), and breast cancer resistance protein (ABCG2) have an effect on olmesartan pharmacokinetics in Korean subjects. Sixty-eight healthy male volunteers who participated in previous pharmacokinetics studies of olmesartan medoxomil (single dose, 20 mg or 40 mg) were enrolled. All subjects were analyzed and grouped according to the genotypes of ABCC2, SLCO1B1, and ABCG2. The dose-normalized peak plasma concentration (C(max)) and area under the plasma concentration-time curve (AUCt) values were analyzed. The dose-normalized mean C(max) and AUC(t) in the ABCC2 -24CT genotype group were higher than those in the -24CC genotype group [C(max,dn): CT 26.1 ± 6.5 (ng/mL)/mg versus CC 22.1 ± 6.7 (ng/mL)/mg, P = 0.010, AUC(t,dn): CT 178.7 ± 45.6 (hr·ng(-1)·mL(-1))/mg versus CC 149.9 ± 39.8 (hr·ng(-1)·mL(-1))/mg, P = 0.010]. The difference in AUC(t,dn) between the ABCC2 -1549GG and -1549GA genotype groups was statistically significant [GG 149.0 ± 41.0 (hr·ng(-1)·mL(-1))/mg versus GA 174.1 ± 43.3 (hr·ng(-1)·mL(-1))/mg, P = 0.019]. No significant differences were observed for any other single nucleotide polymorphism in ABCC2, SLCO1B1, or ABCG2. The ABCC2 -24CC genotype group exhibited lower systemic exposure of olmesartan than the -24CT genotype group, whereas no significant differences were observed in the other transporter genotype groups.

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benicar tablets 2015-01-06

Development of microalbuminuria is a valid marker for future CV events. RAS blockade with Olmesartan might cause sustained reduction (legacy effect) of micro- and macrovascular events. buy benicar

benicar dose 2016-02-02

Goal rates, the percentage of patients with hypertension achieving recommended SBP/DBP, are a clinically important assessment of an antihypertensive agent's efficacy. Twenty-four-hour ambulatory blood pressure monitoring (ABPM) allows accurate assessment of a patient's hypertension and buy benicar risk for cardiovascular events, and provides the most accurate measure of an antihypertensive agent's efficacy throughout a 24-hour dosing interval.

benicar maximum dosage 2015-06-09

Olmesartan and azilsartan, angiotensin II receptor blockers (ARBs), are expected to decrease blood pressure more than the other ARBs. We conducted randomized-controlled trials buy benicar to compare the practical efficacy of olmesartan with azilsartan.

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Following a 2- to 3-week placebo run-in phase, patients received OM 20 mg, uptitrated to OM 40 mg, followed by addition of HCTZ 12.5-25 mg step-wise at 3-week intervals if seated cuff BP (SeBP) was ≥120/70 mmHg. Patients below this target SeBP were maintained at their current dose but uptitrated to the next consecutive dose if mean seated cuff systolic BP (SBP) was ≥140 mmHg and/or mean seated cuff diastolic BP was ≥90 mmHg at follow-up visits. Efficacy buy benicar was assessed by 24-hour ambulatory BP monitoring (ABPM) and SeBP measurements. The primary efficacy variable was the change from baseline in mean 24-hour ambulatory SBP after 12 weeks. Secondary efficacy endpoints included the change from baseline in mean 24-hour ambulatory SBP; change from baseline in ambulatory BP during the daytime (8:00 am-4:00 pm), nighttime (10:00 pm-6:00 am) and the last 6, 4 and 2 hours of the dosing interval; change from baseline in SeBP at each titration step and at study end; and the proportion of patients achieving mean 24-hour ambulatory BP targets and SeBP goals at week 12. The frequency and severity of treatment-emergent adverse events (TEAEs) were also documented.

benicar 10 mg 2015-12-03

Olmesartan may protect the buy benicar spinal cord from I-R injury and reduce the incidence of associated neurological dysfunction after temporary aortic occlusion.

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A total of 205 olmesartan plasma sample concentrations from 69 patients with hypertension were collected in this study. The pharmacokinetic data of olmesartan was well described by a two-compartment linear pharmacokinetic model with first-order absorption and an absorption lag-time. The mean values of CL/F and V/F of olmesartan in the patients were 0.31565 L/h and 44.5162 L, respectively. Analysis of covariates showed that age and CLCR were factors influencing the clearance of olmesartan and the buy benicar volume of distribution of olmesartan was dependent on age and BSA.

benicar medicine 2016-12-14

Based on results of in vitro studies, it has buy benicar been hypothesized that blockade of the renin-angiotensin system (RAS) promotes the recruitment and differentiation of pre-adipocytes and that increased formation of small insulin-sensitive adipocytes counteracts ectopic deposition of lipids, thereby improving insulin sensitivity. We investigated the effect of RAS blockade on insulin sensitivity, adipocyte size, and intramuscular lipid content in fructose-fed rats (FFR) as a model of insulin-resistant hypertension.

benicar 80 mg 2017-03-01

Although fixed-dose combination drug therapy is commonly used to treat hypertension, the efficacy of head-to-head comparisons of dual fixed-dose combinations has not been well described. We hypothesized that when used in combination buy benicar with an angiotensin receptor blocker (ARB) olmesartan medoxomil, hydrochlorothiazide (HCTZ) will be as effective as the dihydropyridine calcium channel blocker (CCB) amlodipine to lower both clinic and 24-h ambulatory blood pressure (BP). Furthermore, we hypothesized that response to ARB along with HCTZ or ARB along with CCB may be heterogeneous depending on clinical characteristics.

benicar dosage 5mg 2017-06-16

Patients with chronic kidney disease (CKD) present a high prevalence of insulin resistance (IR). Some studies suggest that angiotensin II may influence some cellular pathways that contribute to the pathogenesis of IR and stimulate the release of proinflammatory cytokines. Fifty-two patients who had stages 3 and 4 buy benicar CKD and no diabetes were administered an angiotensin receptor blocker (ARB), olmesartan (40 mg), for 16 wk. Before and after ARB treatment, metabolic and inflammatory parameters and adipokines were measured. IR was calculated by Homeostasis Model Assessment (HOMA) index. Baseline data were compared with data that were obtained from 25 healthy control individuals of similar age and normal renal function. Compared with control subjects, patients with CKD presented significantly higher BP and waist circumference, higher triglycerides and lower HDL levels, higher insulin levels, and higher mean HOMA index (6.0 +/- 2.7 versus 2.9 +/- 2.2 muU/ml x mmol/L; P < 0.001). In addition, patients with CKD had increased levels of high-sensitivity C-reactive protein, TNF-alpha, and IL-6. In patients with CKD, leptin was positively correlated to abdominal obesity, insulin levels, and IL-6, and adiponectin was inversely correlated to abdominal obesity and insulin levels. Olmesartan treatment resulted in a significant decrease of BP, urinary protein excretion, plasma glucose (99 +/- 16 versus 92 +/- 14 mg/dl; P < 0.05), insulin (23.1 +/- 8.8 versus 19.9 +/- 9; P < 0.05), HOMA index (6.0 +/- 2.7 versus 4.7 +/- 2.8; P < 0.05), and glycated hemoglobin (5.33 +/- 0.58 versus 4.85 +/- 0.81%; P < 0.01). At the same time, there was a significant reduction of high-sensitivity C-reactive protein levels, from 4.45 mg/L (2.45 to 9.00) to 3.55 mg/L (1.80 to 5.40; P < 0.05) and fibrinogen (412 +/- 100 versus 370 +/- 105 mg/dl; P < 0.05). There were no significant differences in adipokine levels after olmesartan treatment. These data demonstrate that patients with CKD have a high prevalence of IR, metabolic syndrome, and chronic inflammation and that the administration of the ARB olmesartan improves IR and inflammation markers in these patients. Plasma adipokine levels that are related to several metabolic risk factors in patients with CKD were not modified by ARB therapy.

olmesartan benicar cost 2015-12-23

In this prospective, open-label, dose-titration study, patients with uncontrolled BP after at least 1 month of antihypertensive monotherapy were switched to fixed-dose AML/OM 5/20 mg. Patients were uptitrated to AML/OM 5/40 and 10/40 mg, with uptitration to AML/OM + hydrochlorothiazide 10/40 + 12.5 mg and 10/40 + 25 mg to achieve target BP. The primary efficacy endpoint was the cumulative proportion of patients buy benicar achieving seated cuff systolic BP (SeSBP) less than 140 mmHg (<130 mmHg in patients with diabetes mellitus) at 12 weeks. Secondary endpoints included SeBP goal rates, ambulatory BP (ABP) target rates, and mean change from baseline in seated cuff BP (SeBP) and ABP at weeks 12 and 20.

benicar dosage sizes 2017-08-11

Olmesartan has been investigated in several clinical studies. This article reports on data from 1 such study buy benicar with a prospective, randomized, double-blind, placebo-controlled, parallel-group, dose-finding design in patients with mild to moderate hypertension (baseline mean sitting diastolic blood pressure, 100-114 mm Hg). The results from a meta-analysis of 7 randomized, double-blind, placebo-controlled studies are also presented.

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The current preliminary study showed that olmesartan medoxomil treatment might decrease plasma BNP levels, independent of its BP-lowering effect, in hypertensive buy benicar patients with type 2 diabetes.

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ARB improves the overproduction and accumulation of TG in the liver associated with insulin buy benicar resistance, and does so through mechanisms independent of its hypotensive action.

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The authors examined the effects of olmesartan-based treatment on clinic systolic blood pressure (CSBP) and morning home systolic blood pressure (HSBP) in 21,340 patients with masked hypertension (MH), white-coat hypertension (WCH), poorly controlled hypertension (PCH), and well-controlled hypertension (CH) using data from the Home Blood Pressure Measurement With Olmesartan Naive Patients to Establish Standard Target Blood Pressure (HONEST) study. MH, WCH, PCH, and CH were defined using CSBP 140 mm Hg and MHSBP 135 mm Hg as cutoff values at baseline. At 16 weeks, the MH, WCH, PCH, and CH groups had changes in CSBP by -1.0, -15.2, -23.1 buy benicar , and 1.8 mm Hg, and changes in morning HSBP by -12.5, 1.0, -20.3, and 2.0 mm Hg, respectively. In conclusion, in "real-world" clinical practice, olmesartan-based treatment decreased high morning HBP or CBP without excessive decreases in normal morning HBP or CBP according to patients' BP status.

benicar maximum dose 2017-11-18

Angiotensin II plays an Protonix 70 Mg important role in cardiac hypertrophy or remodeling. Angiotensin II receptor blockers (ARB) are clinically useful for the treatment of hypertension and heart failure. However, the molecular effects of ARB in the mechanically-stressed myocardium have not been completely defined. We investigated the effects of ARB on mechanically-modulated genes in cardiac myocytes.

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This subanalysis of the OLMETEL (OLMEsartan TELemonitoring blood pressure) study in patients with essential hypertension assessed the relationship between the frequency of blood pressure self-measurement (BPSM) and the response to blood pressure (BP)-lowering therapy with olmesartan Cytoxan Pill medoxomil, and the number of BP readings per week necessary to detect a mean systolic or diastolic BP reduction > or =5mm Hg.

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Patients were randomized to 24 weeks of treatment with either olmesartan medoxomil 20 mg daily (n = 256) or nitrendipine 20 mg (n = 126) twice daily, with possible dose increase (to 40 mg daily) and addition of hydrochlorothiazide (HCTZ) 12.5 or Paracetamol 500mg Tablets 25 mg daily if required.

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Randomised, double- Ceftin Medication blind, parallel-group study conducted at 44 centres in Germany, Poland and the Czech Republic.

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Cerebrovascular and cardiac adverse events can be significantly reduced by effective antihypertensive therapy; however, BP control rates remain poor. The objective of this randomized, double-blind, parallel-group, multicentre study was to determine the efficacy and safety of olmesartan medoxomil/amlodipine combination therapy in patients with moderate to severe hypertension who had Cymbalta Dosage Amounts failed to respond to treatment with 8 weeks of open-label amlodipine.

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Olmesartan and atenolo produced comparable significant reductions in CC-IMT; mean Delta IMT (SEM) was -0.090 (0.015) mm for oLmesartan and -0.082 (0.014) mm for atenolol. Mean Delta PV was -4.4 (2.3) microl and 0.1 (1.5) microl in the olmesartan and atenolol treated subjects, respectively, without significant between-treatment differences. In the subgroup of patients with baseLine PV > or = median (33.7 microl), significant between-treatment differences existed in Delta PV (p = 0.023), because PV regressed significantly with olmesartan (Delta PV: -11.5 (4. Famvir Buy Online 4) microl) but not with atenolol ( Delta PV: 0.6 (2.5) microl). In these patients BP reductions were comparabLe.

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We investigated the effects of an angiotensin-converting enzyme inhibitor (temocapril) and an angiotensin II type 1 receptor blocker (olmesartan) on changes in myocardial sympathetic nervous activity, fatty acid metabolism and myocardial blood flow using 131I-meta-iodobenzylguanidine, 125I-beta-methyl-iodophenyl pentadecanoic acid and 99mTc-tetrofosmin, respectively, in rats with isoproterenol-induced cardiac hypertrophy. Male Sprague-Dawley rats underwent isoproterenol administration (3 mg/kg per day) for 1 week by osmotic mini-pump. The hearts were excised and analyzed for the uptake of meta-iodobenzylguanidine. Beta-methyl-iodophenyl pentadecanoic acid and tetrofosmin in 11 segments in four groups; sham group (saline), isoproterenol group (isoproterenol alone), angiotensin-converting enzyme inhibitor group (isoproterenol and temocapril), and angiotensin II type 1 receptor blocker group (isoproterenol and olmesartan). Isoproterenol significantly increased the heart weight compared with the sham group, whereas it was significantly blunted in the angiotensin-converting enzyme inhibitor and angiotensin II type 1 receptor blocker groups. The ratio of the percent kilogram dose per gram of meta-iodobenzylguanidine to tetrofosmin, an index of myocardial sympathetic nervous activity, was significantly decreased in the isoproterenol group (0.18 +/- 0.01) compared with the sham group (0.41 +/- 0.03). Importantly, these changes were significantly improved in the angiotensin-converting enzyme inhibitor (0.28 +/- 0.01) and the angiotensin II type 1 receptor blocker groups (0.32 +/- 0.01). The ratio of the percent kilogram dose per gram of beta-methyl-iodophenyl pentadecanoic acid to tetrofosmin, an index of myocardial fatty acid metabolism, was significantly decreased in the isoproterenol group (1.30 +/- 0.03) compared with the sham group (1.60 +/- 0.10). In contrast, there were no significant differences in beta-methyl-iodophenyl pentadecanoic acid to tetrofosmin ratios between the sham and angiotensin-converting enzyme inhibitor groups, or the angiotensin II type 1 receptor blocker group. Cardiac hypertrophy induced by chronic beta-adrenergic stimulation is accompanied by impairment of sympathetic nervous Claritin Tablets activity and fatty acid metabolism. These abnormalities are effectively prevented by the angiotensin-converting enzyme inhibitor and the angiotensin II type 1 receptor blocker.

benicar hct medication 2015-07-07

Both olmesartan and Avapro Dose azilsartan equally reduced blood pressures. Both olmesartan and azilsartan showed a renoprotective effect and were well tolerated without any major adverse events.

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Mean SeBP was 158.1/90.0 mmHg at baseline. The mean ± standard error of BP reductions at 12 weeks for systolic and diastolic BP were 21.3 ± 1.1 mmHg and 9.8 ± 0.6 mmHg Bactrim Oral Medication , respectively (p < 0.0001 for each). At the end of the study, the proportion of patients with diabetes achieving the recommended SeBP goal of <130/80 mmHg was 41.1%.

benicar generic equivalent 2015-10-15

The absorption process in animals of TAK-491, designed as ester-based prodrug with medoxomil moiety, was evaluated. In the plasma of rats and dogs, TAK-536, the pharmacologically active metabolite, was present as the main component with hardly detectable concentrations of TAK-491 after oral administration of TAK-491. In the rat portal plasma, TAK-536 was also present as the main component with hardly detectable concentrations of TAK-491 after jejunal loop injection of TAK-491, suggesting TAK-491 was absorbed from small intestine and hydrolyzed almost completely during absorption. Caco-2 study indicated the permeability of TAK-491 was improved by prodrug modification and the compound could be mainly transferred as TAK-491. This is well consistent with the facts that the AUC and T(max) of TAK-536 after oral administration of TAK-491 were higher and shorter than those after oral administration of TAK-536 in dogs Hydrolysis of TAK-491 is observed not only by the intestinal and hepatic S9 fraction, but also by plasma and human serum albumin. However, medoxomil alcohol wasn't detected during the hydrolysis of TAK-491. These metabolic features of TAK-491 were similar to olmesartan medoxomil, suggesting the hydrolytic pathway and enzymes for TAK-491 when catalyzing to TAK-536 would be the same as olmesartan medoxomil.

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(1) Atenolol and OM both reduced BP effectively in moderate to severe hypertensives. OM was significantly superior to: (2) losartan (95% confidence interval for baseline to week 12 change in DBP < 0, lower limit < -3.6 mmHg); and (3) captopril (95% confidence interval for baseline to week 12 change in DBP < 0, lower limit < -4.8 mmHg) in BP reduction for mild to moderate hypertensives. Treatment with OM was safe and well tolerated.