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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:
Almetec, Alteis, Benetor, Cardioplus, Olmec, Olmes, Olmesartan, Olmesartana, Olmesartanum, Olmetec, Olpress, Olprezide, Olsar, Omesar, Openvas, Orizal, Plaunac, Plaunazide, Revival, Sevikar, Tensar, Tensiol, Tensonit, Tespadan, Vascord, Vocado, Votum

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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.

Side effects

The most common side effects associated with Benicar 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 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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The interest for powerful and better tolerated antihypertensive combinations is searched in the field of hypertension, because of a too large number of people still not well controlled. The recent association between an angiotensin receptor blocker, olmesartan, and a long-acting dihydropyridine, amlodipine, reinforces our therapeutic possibilities. The synergistic effect of the two molecules potentiate the antihypertensive activity, which allows improving the quality and the rapidity of the blood pressure control. Furthermore, the fixed combination should improve patient's compliance. The contraindications still remain those of the sartan family. The most frequent side-effect of amlodipine monotherapy, oedema, occurs in a much lower proportion with the addition of olmesartan.

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Casual blood glucose level was associated with the duration of treatment (P < 0.0001), but not with age, sex, or medication. Blood glucose level was significantly decreased during the periods of 0~3 months (P < 0.0001) and 3~6 months (P = 0.0081) compared with baseline, but was not significantly different between 6~12 months and baseline. There was no association between HbA1c level and covariates of sex, age, medication and duration of treatment.

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We administered ARBs (olmesartan, candesartan, and telmisartan) to mice and evaluated antigen-specific T cell proliferation and cytokine production following immunization with ovalbumin (OVA) or type II collagen in Freund's complete adjuvant (CFA) or aluminum hydroxide (alum). Next, we induced CIA in DBA/1 mice and administered olmesartan. The severity and incidence of arthritis were scored according to clinical manifestations, and joint tissue sections were examined histopathologically.

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The therapeutic profile of olmesartan medoxomil, which is a recently developed angiotensin II (A II) receptor blocker, has been compared with four commonly used antihypertensive therapeutic drugs (atenolol, captopril, felodipine and losartan) in five separate multicentre, randomised, double-blind, parallel-group, phase III trials. The trials were designed to compare the efficacy of individually optimised dosages of olmesartan medoxomil and the comparator agent. The primary efficacy variable in all trials was the mean change from baseline to week 12 in trough mean sitting diastolic blood pressure (DBP). Olmesartan medoxomil (10-20 mg once daily (o.d.)) showed similar efficacy to atenolol (50-100 mg o.d.), both in patients with mild-to-moderate hypertension and, when given together with hydrochlorothiazide (HCTZ) 25 mg o.d., in patients with moderate-to-severe hypertension. Olmesartan medoxomil (20-40 mg o.d.) was also similar in efficacy to felodipine (5-10 mg o.d.) in reducing BP in patients with mild-to-moderate hypertension. Compared with captopril (12.5-50 mg twice daily (b.i.d.)) and losartan (50-100 mg o.d.), in patients with mild-to-moderate hypertension, olmesartan medoxomil (5-20 mg o.d. and 10-20 mg o.d., respectively) was significantly superior in terms of lowering DBP from baseline to week 12. In terms of the secondary efficacy variable, which was mean change from baseline to week 12 in trough mean sitting systolic BP, olmesartan showed significant superiority to atenolol, captopril and losartan in patients with mild-to-moderate hypertension. In the longer term, compared with losartan, a lower percentage of olmesartan-treated patients required concomitant HCTZ after 12 weeks of therapy. Olmesartan was well tolerated in all studies.

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We recruited 25 patients to study our hypothesis. All had a history of stroke or silent cerebral infarction. We switched them to olmesartan (10-40 mg per day) for 12 weeks and determined their plasma level of Ang-(1-7), peroxiredoxin, oxidized low-density lipoprotein (oxLDL)/β-2-glycoprotein I (β2GPI) complex, adiponectin, high mobility group box 1 (HMGB1), and tumor necrosis factor-α (TNFα) and recorded their BP before and after olmesartan treatment.

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Six-week-old male Sprague-Dawley rats were divided into two groups: those fed a standard chow (control) and those fed a fructose-rich chow for 6 weeks. FFR were treated with a vehicle or with 1 mg/kg per day of temocapril, an angiotensin-converting enzyme inhibitor, or 0.1 mg/kg per day of olmesartan, an angiotensin II type 1 receptor blocker, for the last 2 weeks. Insulin sensitivity (M value: mg/kg per min) was estimated by the euglycemic hyperinsulinemic glucose clamp method. Sizes of adipocytes derived from epididymal fat and triglyceride content in the soleus muscle were determined.

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To assess the efficacy and safety of once daily olmesartan medoxomil (OM)/amlodipine besylate (AM)/hydrochlorothiazide (HCTZ) 40/10/25 mg in patients with hypertension not at goal with mono, dual or triple drug therapy.

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One thousand seven hundred and fifty-eight ROADMAP patients (placebo arm: 877; OM arm: 881) participated in the observational follow up (OFU) with an average of 3.3 years. They received standard medical care and micro- and macrovascular events were documented. During observational follow-up 62.9% and 60.1% in the former OM and placebo group, respectively, received treatment with a RAS blocking agent. During the OFU period the systolic blood pressure (SBP) increased to mean values of 135 mm Hg in both groups. Patients who had developed microalbuminuria during ROADMAP had a higher incidence of cardio- and cerebrovascular events (OR 1.77, CI 1.03 to 3.03, P=0.039) during the OFU period compared with patients in whom this was not the case. Diabetic retinopathy was significantly reduced in the former OM group (8 [0.9%] versus 23 [2.6%], OR: 0.34, CI 0.15 to 0.78, P=0.011) and the rate of microalbuminuria was numerically reduced. Congestive heart failure requiring hospitalization (3 [0.3%] versus 12 [1.4%], OR: 0.23, CI 0.06 to 0.85, P=0.027) was reduced and there was a trend of reduced cardio-/cerebrovascular events (OM versus Pb: 73 [8.3%] versus 86 [9.8%] patients). Seven (0.8%) deaths (including 2 CV events) were reported in former placebo patients versus 3 (0.3%) (non-CV events) in former OM patients.

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A total of 18 diurnally active subjects with uncomplicated, mild to moderate, essential hypertension were studied to compare the efficacy of the morning versus evening administration of an oral olmesartan medication. After a two-week, wash-out/placebo run-in period, subjects with clinic diastolic blood pressure (DBP) > or = 90 mm Hg and <110 mm Hg began 12 weeks of 20 mg olmesartan medoxomil tablet therapy at 08:00 h daily. Four of the 18 subjects required dose escalation to 40 mg at eight weeks because of clinic DBP > or = 90 mm Hg. After the 12-week period of once-a-day 08:00 h treatment, subjects were immediately switched to an evening (20:00 h) drug-ingestion schedule for another 12-week period without change in dose. Subjects underwent 24 h ambulatory blood pressure monitoring (ABPM) before the initiation of morning treatment and at the end of both the 12-week morning and evening treatment arms. Dosing time did not exert statistically significant differences on the efficacy of olmesartan: the reduction from baseline in the 24 h mean systolic (SBP) and DBP was, respectively, 18.8 and 14.6 mm Hg with morning dosing and 16.1 and 13.2 mm Hg with evening dosing (p>0.152 between groups). The amplitude of the BP 24 h pattern did not vary with dosing time, indicating full 24 h BP reduction no matter the clock hour of treatment. Although, the BP-lowering effect was somewhat better with morning dosing, the results of this study suggest that the studied olmesartan medoxomil preparation efficiently reduces BP when ingested in the morning (08:00 h) or evening (20:00 h) in equivalent manner, based on statistical testing, throughout the 24 h.

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We measured a panel of vascular inflammation markers, including high-sensitivity C-reactive protein, and lipid levels during 12 weeks of therapy with olmesartan (n=100) or placebo (n=99) in a prospective double-blind multicenter study. Pravastatin was added to the double-blind therapy at week 6 in both treatment arms. Blood pressure control was achieved with addition of hydrochlorothiazide. Olmesartan treatment had already significantly reduced serum levels of high-sensitivity C-reactive protein (-15.1%; P<0.05), high-sensitivity tumor necrosis factor-alpha (-8.9%; P<0.02), interleukin-6 (-14.0%; P<0.05), and monocyte chemotactic protein-1 (-6.5%; P<0.01) after 6 weeks of therapy, whereas placebo treatment (ie, blood pressure reduction) had no major effect on inflammation markers. After 12 weeks of therapy, high-sensitivity C-reactive protein (-21.1%; P<0.02), high-sensitivity tumor necrosis factor-alpha (-13.6%; P<0.01), and interleukin-6 (-18.0%; P<0.01) decreased further with olmesartan and pravastatin cotherapy, but treatment with pravastatin alone (ie, cotherapy with placebo) did not significantly alter inflammation markers. In contrast, addition of pravastatin led to a significant (P<0.001) reduction in LDL cholesterol serum concentrations in the olmesartan and placebo treatment groups (-15.1% and -12.1%, respectively).

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Individuals > or =18 years of age with mean seated blood pressure (BP) > or =140/100 or > or =160/90 mm Hg divided into Hispanic/Latino (369) and non-Hispanic/Latino (2122) subgroups.

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Hypertension is a major risk factor for cardiovascular disease that contributes to the premature death of millions of people each year, and identification and treatment of hypertension continues to be a challenge. Guidelines recommend that many patients will require two or more antihypertensive agents from different classes. Combining an angiotensin II receptor blocker (ARB) with hydrochlorothiazide (HCTZ) has been shown in clinical studies to increase the antihypertensive efficacy of both agents compared with either agent alone. This review covers several clinical trials and aims to examine several aspects of the efficacy of the combination of olmesartan and HCTZ, including dose-responsiveness, long-term efficacy, goal rate achievement, and efficacy in patients with moderate to severe hypertension. The results presented here demonstrate that olmesartan is effective when added to HCTZ monotherapy or when HCTZ is added to olmesartan monotherapy, both over the short and long term. Moderate to severe hypertension responds well to olmesartan/HCTZ combination therapy, and the great majority of patients are able to achieve recommended blood pressure targets. Thus olmesartan/HCTZ is a well-tolerated option for patients who fail to respond to monotherapy and as initial therapy in those who require large reductions in diastolic blood pressure or systolic blood pressure to achieve goal blood Generic Suprax Cefixime Tablet pressure.

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Effective treatment of high blood pressure represents a key strategy for reducing the burden of hypertension-related cardiovascular diseases. In spite of these well-established concepts, hypertension remains poorly controlled worldwide. In addition, treated hypertensive patients often remain at higher risk compared with the normotensive population, even when a satisfactory blood pressure control is achieved, owing to a high or very high added cardiovascular risk profile. An emerging strategy to improve blood pressure control in hypertensive patients Lanoxin Generic is a more extensive use of combination therapy than monotherapy in the daily clinical practice. Within the possible antihypertensive drug combinations currently available for the clinical management of hypertension, those based on the association of drugs inhibiting the renin-angiotensin system and thiazide diuretics or calcium channel-blockers have demonstrated to be effective and safe in lowering both systolic and diastolic blood pressure levels with a good tolerability profile. This article provides an overview of fixed-combination strategies, with a particular focus on the fixed-combination strategies based on olmesartan medoxomil.

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Twenty-one healthy male subjects (mean age, 21 years [range, 18-25 years]; weight, 62.1 kg [range, 54.0-80.0 kg]) were enrolled in and completed the study. No period or sequence effect was observed. The mean AUC(0-∞) values for the test tablet, test capsule, and reference tablet were 3993 (1070), 3567 (850), and 3849 (872) ng/mL/h, respectively. The 90% CIs for the log-transformed ratios of test tablet to reference tablet for C(max), AUC(0-48), and AUC(0-∞) were 103.9 to 124.9, 94.0 to 111.5, and 94.4 to 111.7, respectively (all, P = NS). The corresponding 90% CIs for the log-transformed ratios of test capsule to reference tablet were 90.8 to 109.2, 84.9 to 107.9, and 85.1 to 100.7 (all, P = NS). Ten adverse events were reported during the study; Rosuvastatin Crestor Generic 7 subjects complained of pain during blood sampling, and 3 had a blocked venous catheter. No treatment-related adverse events were reported or observed.

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Endothelial dysfunction is the common link between cardiovascular disease risk factors and the earliest event in the cascade of incidents that results in target organ damage. Angiotensin II, the terminal pressor effector arm of the renin-angiotensin-aldosterone system, increases blood pressure (BP) by vasoconstriction and sodium and fluid retention, and has a pro-oxidative action that induces endothelial dysfunction and contributes to vascular remodeling. Angiotensin receptor blockers (ARBs) reduce BP and morbidity and mortality in patients with hypertension, ventricular hypertrophy, diabetes mellitus, and renal disease. Olmesartan medoxomil is a long-acting, well- Myambutol Cost tolerated, effective ARB that prevents or reverses endothelial dysfunction in animal models of atherosclerosis, hypertension, diabetes, nephropathy, and retinopathy. Olmesartan medoxomil, a prodrug of olmesartan approved for the treatment of hypertension, has been shown to ameliorate endothelial dysfunction in patients with hypertension or diabetes. In randomized studies, the drug reduces vascular inflammation and the volume of large atherosclerotic plaques, increases the number of regenerative endothelial progenitor cells in the peripheral circulation, improves endothelium-dependent relaxation, and restores the normal resistance vessel morphology. Importantly, the impact of olmesartan medoxomil on endothelial dysfunction is thought to be independent of BP lowering.

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In the ARB group, a significant decrease in CAVI was observed after 12 months; however, no significant change in CAVI was observed in the Ca blocker group although changes in blood pressure were almost the same. By simple regression analyses, CAVI changes correlated positively with 8-OHdG Vytorin Generic Release Date changes.

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FFR had lower M value, higher blood pressure, larger adipocyte size, higher ratio of epididymal fat pads over body weight (%fat pads), and higher intramuscular triglyceride than did the control rats. Both temocapril and olmesartan significantly improved the M value and decreased blood pressure and adipocyte size without change in %fat pads in FFR. Adipocyte Diovan 320 Generic size was negatively correlated with the M value. Treatment for 2 weeks decreased, but not significantly, intramuscular triglyceride.

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In the intention-to-treat population (542 patients O and 539 R) after 12 weeks of treatment baseline-adjusted office SBP and DBP reductions were greater (P < 0.01) with O [17.8 (95% confidence interval: 16.8/18.9) and 9.2 (8.6/9.8) mmHg] than with R [15.7 (14.7/16.8) and 7.7 (7.1/8.3) mmHg]. BP normalization rate was also greater under O (52.6 vs. 46.0% R, P < 0.05). In the subgroup of patients with valid ambulatory BP recording (318 O and 312 R) the reduction in 24-h average Avalide Generic Price BP was larger (P < 0.05) with O [SBP: 11.0 (12.2/9.9) and DBP: 6.5 (7.2/5.8) mmHg] than with R [9.0 (10.2/7.9) and 5.4 (6.1/4.7) mmHg]. The larger blood pressure reduction obtained with O was particularly evident in the last 6 h from the dosing interval; a better homogeneity of the 24-h BP control with O was confirmed by higher smoothness indices. The proportion of patients with drug-related adverse events was comparable in the two groups (3.6 O vs. 3.6% R), as well as the number of patients discontinuing study drug because of a side effect (14 O vs. 19 R).

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Both treatments similarly reduced the blood pressure, improved survival and ameliorated LV enlargement. In contrast, several parameters of LV function were significantly ameliorated only by the high-dose ACE-I but not Keflex Generic by the combination therapy.

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Olmesartan medoxomil provides a more effective and sustained 24-h BP control than ramipril in elderly hypertensive patients, particularly in the hours farthest from Micardis Generic Availability last intake.

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Recent studies have indicated that both endothelin (ET) and angiotensin (Ang) II stimulate oxidative stress, which contributes to the development of hypertension. Here, we examined the effects of Ang II type 1 (AT1) receptor blockade on reactive oxygen species (ROS) formation in ET-dependent hypertension. Chronic ET-1 infusion (2.5 pmol/kg/min, i.v., n=7) into rats for 14 days increased systolic blood pressure from 113+/-1 to 141+/-2 mmHg. ET-1-infused rats showed greater plasma renin activity (8.1+/-0.8 Ang I/ml/h), and greater Ang I (122+/-28 fmol/ml) and Ang II levels (94+/-13 fmol/ml) than vehicle (0.9% NaCl)-infused rats (3.1+/-0.6 Ang I/ml/h, 45+/-8 and 47+/-7 fmol/ml, respectively, n=6). Angiotensin converting enzyme and AT1 receptor expression in aortic tissues were similar between the vehicle- and ET-1-infused rats. Vascular superoxide anion (O2-) production and plasma thiobarbituric acid-reactive substance (TBARS) levels were greater in ET-1-infused rats (27+/-1 counts per minutes [CPM]/mg dry tissue weight and 8.9+/-0.8 micromol/l, respectively) than vehicle-infused rats (16+/-1 CPM/mg and 5.1+/-0.1 micromol/l, respectively). The ET-1-induced hypertension was prevented by simultaneous treatment with a new AT1 receptor antagonist, olmesartan (0.01% in chow Zetia 10mg Generic , 117+/-5 mmHg, n =7), or hydralazine (15 mg/kg/day in drinking water, 118+/-4 mmHg, n=6). Olmesartan prevented ET-1-induced increases in vascular O2- production (15+/-1 CPM/mg) and plasma TBARS (5.0+/-0.1 micromol/l). Vascular O2- production and plasma TBARS were also decreased by hydralazine (21+/-1 CPM/mg and 7.0+/-0.3 micromol/l, respectively), but these levels were significantly higher than in vehicle-infused rats. These data suggest that ET-dependent hypertension is associated with augmentation of Ang II levels and ROS formation. The combined effects of the elevations in circulating ET-1 and Ang II, as well as the associated ROS production, may contribute to the development of hypertension induced by chronic ET-1 infusion.

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In the total cohort, olmesartan 20 and 40 mg/day resulted in mean reductions in SBP of 15.1 and 17.6 mm Hg, respectively (P < .001 v placebo). In the wide PP cohort, olmesartan resulted in mean reductions in SBP of 17.7 and 22.0 mm Hg and mean reductions in PP of 7.4 Hg and 8.8 mm Hg for the groups receiving 20 and 40 mg/day, respectively (P < .001 v placebo). In the cohort with wide PP and age > or = 65 years, olmesartan 20 and 40 mg/day produced mean reductions in SBP of 21.8 and 22.5 mm Hg, and PP of 6.7 and 7.6 mm Hg, respectively (P < .05 v placebo).