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:
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.
The most common side effects associated with Benicar are:
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 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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Cardiorenal metabolic syndrome (CRS) is a global health care concern in view of aging in certain populations, increased obesity, changing lifestyles, and its close association with type 2 diabetes mellitus and cardiovascular morbidity and mortality. Determining the appropriate criteria for CRS has been somewhat controversial, and efforts to fully describe and define the syndrome are still ongoing. Nonetheless, improving knowledge of the syndrome among health care professionals will help to identify patients who may require pharmacological and therapeutic lifestyle intervention, particularly with regards to addressing high-normal blood pressure and hypertension. This article reviews current clinical guidelines with a focus on the identification, especially in racial/ethnic minorities, treatment, and associated cardiovascular morbidity and mortality of high blood pressure and hypertension in patients with CRS. Efficacy and outcomes studies that provide insight into the selection of an initial antihypertensive regimen in this population will be discussed. Finally, a brief review of the benefits of olmesartan medoxomil and combination therapy and patient factors in the management of hypertension with CRS will be addressed.
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The attainment of clinical blood pressure (BP) goals can markedly reduce cardiovascular morbidity and mortality, yet approximately two-thirds of treated hypertensive patients in the United States have uncontrolled BP. Consequently, more aggressive management of hypertension, frequently involving combination therapy (e.g., fixed-dose combination [FDC] therapy), is needed to achieve the recommended BP goals of <140/90 mmHg for most patients, and <130/80 mmHg for high-risk patients.
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12B75, 274150; Abacavir sulfate/lamivudine, Abatacept, Ad2/HIF-1alpha, Adalimumab, Adefovir, Adefovir dipivoxil, AGN-201904-Z, AIDSVAX, Albinterferon alfa-2b, Alemtuzumab, Aliskiren fumarate, Alvimopan hydrate, Amlodipine besylate/atorvastatin calcium, Amlodipine besylate/Olmesartan medoxomil, Ammonium tetrathiomolybdate, Amodiaquine, Apaziquone, Aprepitant, Arsenic trioxide, Artesunate/Amodiaquine, Ascorbic acid, Atazanavir sulfate, Atazanavir/ritonavir, Atomoxetine hydrochloride, Atrigel-Leuprolide, Axitinib; Bevacizumab, Binodenoson, Bortezomib, Bovine lactoferrin; Calcipotriol/betamethasone dipropionate, Carisbamate, Certolizumab pegol, Ciclesonide, Conivaptan hydrochloride, CP-690550, CP-751871, Cypher; Dapivirine, Darbepoetin alfa, Darunavir, Dasatinib, del-1 Genemedicine, Denosumab, Desloratadine, Dexlansoprazole, DiabeCell, Drospirenone/ethinylestradiol, DTaP-HepB-IPV, Duloxetine hydrochloride, Dutasteride; Eculizumab, Eldecalcitol, Eletriptan, Emtricitabine, Entecavir, Eritoran tetrasodium, Ertapenem sodium, Escitalopram oxalate, Eslicarbazepine acetate, Esomeprazole magnesium, Estradiol acetate, Eszopiclone, ETEC vaccine, Etoricoxib, Exenatide, Ezetimibe; Fluticasone furoate, Fosmidomycin, Fosmidomycin/clindamycin; Glutamine; Heat Shock Protein 10, Hepatitis B hyperimmunoglobulin, HIV vaccine, Hochuekki-to, Human Albumin, Human papillomavirus vaccine; Immune globulin subcutaneous [human], IMP-321, Interferon omega, ISIS-301012, Istaroxime; Japanese encephalitis virus vaccine; Latanoprost/timolol maleate, Lenalidomide, Linaclotide acetate, Lumiracoxib, LY-517717; Malaria vaccine, MAS-063D, Meningitis B vaccine, Mepolizumab, Methylnaltrexone bromide, Micafungin sodium, MK-0822A, Morphine glucuronide, Morphine hydrochloride, Mycophenolic acid sodium salt; Natalizumab, Nesiritide, Norelgestromin/ethinyl estradiol, NT-201; Oblimersen sodium, Olmesartan medoxomil, Olmesartan medoxomil/hydrochlorothiazide, Omalizumab, Otamixaban; Paclitaxel nanoparticles, Panitumumab, Panobinostat, Parathyroid hormone (human recombinant), Parecoxib sodium, Pegfilgrastim, Peginterferon alfa-2a, Peginterferon alfa-2b, Pegvisomant, PI-88, Pimecrolimus, Pneumococcal 7-valent conjugate vaccine, Pneumococcal 9-valent conjugate vaccine, Pneumococcal conjugate vaccine, Poloxamer-188, Prasugrel, Pregabalin, Prulifloxacin; R-109339, Ramipril/amlodipine, Ranolazine, Rasburicase, rHA influenza vaccine, Ro-50-3821, Rosuvastatin calcium, Rotavirus vaccine, Rotigotine, Ruboxistaurin mesilate hydrate; Satavaptan, SC-75416, Solifenacin succinate, Sorafenib, Sugammadex sodium, Sunitinib malate, Synthetic conjugated estrogens B; Tadalafil, Talnetant, Taxus, Tegaserod maleate, Telbivudine, Temsirolimus, Tenofovir disoproxil fumarate, Tetomilast, Tiotropium bromide, Tipifarnib, Tofimilast, Tremelimumab, Trimethoprim; Udenafil, Urocortin 2; Valdecoxib, Vernakalant hydrochloride; XP-828L.
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Triple-drug therapy vs the dual therapies resulted in greater mean reduction in SeBP (Hispanic/Latino: 35.0/20.9 mm Hg vs 27.8-30.9/15.3-17.7 mm Hg; non-Hispanic/Latino: 39.0/21.7 mm Hg vs 28.9-31.5/14.6-17.8 mm Hg) and enabled more participants to reach BP goal (Hispanic/Latino: 56.8% vs 40.6%-51.2%; non-Hispanic/Latino: 65.7% vs 33.8%-46.6%) irrespective of ethnicity. The efficacy of triple-drug therapy in achieving BP goal was sustained long-term (40-week open-label extension period) in Hispanic/Latino (63.3%) and non-Hispanic/ Latino (64.2%) participants. Triple-drug therapy was well tolerated in Hispanic/Latino and non-Hispanic/Latino participants.
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Angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) have been shown to be effective and well tolerated in hypertensive patients. Olmesartan is the seventh angiotensin receptor blocker licensed by the US Food and Drug Administration. The aim of this meta-analysis was to determine the efficacy and tolerability of olmesartan medoxomil in comparison with other ARBs.
Olmesartan medoxomil 20-40 mg once daily reduced the systolic/diastolic ambulatory BP for 24-h, daytime, and night-time by 13.3 ± 16.3/7.6 ± 9.5, 13.9 ± 17.4/8.0 ± 10.4, and 12.3 ± 18.1/6.8 ± 10.2 mmHg in all eligible patients at week 24 from baseline (n = 87, P < 0.0001). The global and individual T/P ratios were 0.64/0.62 and 0.32/0.30 (n = 87) for systolic/diastolic BP, whereas these were 0.71/0.70 and 0.31/0.39 in fair responders (n = 71). Global and individual SI were 6.81/5.37 and 0.92/0.67 (n = 87) for systolic/diastolic BP, whereas these were 7.04/5.44 and 1.03/1.03 in fair responders (n = 71). Global and individual T/P ratios for systolic/diastolic BP were 0.75/0.82 and 0.45/0.46 in the 20 mg subgroup (n = 41), whereas these were 0.44/0.59 and 0.30/0.29 in the 40 mg subgroup (n = 30). Global and individual SI were 5.70/5.32 and 1.03/0.87 for systolic/diastolic BP in the 20 mg subgroup (n = 41), but these were 3.64/2.46 and 1.01/0.60 in the 40 mg subgroup (n = 30).
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The prevalence of isolated systolic hypertension (ISH) is high in the elderly, and the objective of this study was to compare the antihypertensive efficacy of olmesartan medoxomil with that of nitrendipine in elderly (65-74 years) and very elderly (>/= 75 years) male and female patients with ISH.
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To compare the relative efficacy and safety of olmesartan medoxomil (OM) with atenolol, captopril and losartan in phase III trials on mild to severely hypertensive patients.
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Following cerebral ischemia, i.v. infusion of angiotensin II increases cerebral edema and mortality. Angiotensin type 1 receptor blockage should therefore improve acute cerebral ischemia. Left middle cerebral artery occlusion (120 min) followed by reperfusion was performed with the thread method under halothane anesthesia in Sprague-Dawley rats. Olmesartan (angiotensin type 1 receptor blocker; 0.01 or 0.1mumol/kg/h) was infused i.p. for 7 days following middle cerebral artery occlusion followed by reperfusion. Stroke index score, infarct volume, specific gravity, and brain angiotensin II and matrix metalloproteinases were quantified in the ischemic and non-ischemic hemispheres. Olmesartan treatment improved stroke index score, infarct volume, and cerebral edema in our cerebral ischemia model. In particular, stroke index score, infarct volume, and cerebral edema were reduced even with a low dose of olmesartan that did not decrease blood pressure. Paralleling these effects on cerebral ischemia, olmesartan treatment also reduced the reactive upregulation in brain angiotensin II, matrix metalloproteinase-2, matrix metalloproteinase-9, and membrane type 1-matrix metalloproteinase in the ischemic area. Angiotensin type 1 receptor stimulation may be one of the important factors that cause cerebral edema following cerebral ischemia, and that its inhibition may be of therapeutic advantage in cerebral ischemia.
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This was a multicenter, randomized, double-blind, placebo-controlled, factorial study. Patients who were naive to antihypertensive therapy or who underwent a washout of previous antihypertensive therapy for up to 2 weeks and had a seated diastolic BP (SeDBP) of 95 to 120 mm Hg were randomized to receive 1 of the following for 8 weeks: OM 10, 20, or 40 mg; amlodipine (AML) 5 or 10 mg; each possible combination of OM and AML; or placebo. The primary end point was the change from baseline in SeDBP at week 8, with secondary end points including the change in seated systolic blood pressure (SeSBP), the proportion of patients reaching the BP goal (<140/90 mm Hg; <130/80 mm Hg for patients with diabetes), and the proportions of the intention-to-treat population reaching BP thresholds of <120/80, <130/80, <130/85, and <140/90 mm Hg. Safety and tolerability were also evaluated, with a particular focus on the incidence and severity of edema.
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European hypertension guidelines estimate that up to 15-20% of hypertensive patients are not controlled on a dual antihypertensive combination and require three or more different antihypertensive drug classes to achieve blood pressure (BP) control.
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Combination of olmesartan medoxomil (10-40 mg) with amlodipine 5 mg for 8 weeks (double-blind) reduced mean SBP/DBP by up to 16.8 mmHg and 9.6 mmHg, respectively. The additional adjusted mean change in seated DBP (SeDBP) [primary endpoint] with last observation carried forward (LOCF) compared with placebo/amlodipine 5 mg was -2.0 mmHg (p = 0.0207), -3.7 mmHg (p < 0.0001) and -3.8 mmHg (p < 0.0001) for olmesartan medoxomil/amlodipine 10/5 mg, 20/5 mg and 40/5 mg, respectively. The corresponding additional adjusted mean change in SeSBP compared with placebo/amlodipine 5 mg was -3.5 mmHg (p = 0.0103), -5.8 mmHg (p < 0.0001) and -7.1 mmHg (p < 0.0001) for the olmesartan medoxomil/amlodipine 10/5 mg, 20/5 mg and 40/5 mg groups, respectively. Uptitration was associated with further mean reductions of up to 12.6 mmHg (SeSBP) and 8.2 mmHg (SeDBP), and allowed additional patients to achieve goal BP. Target BP was defined using both SBP and DBP criteria (patients without diabetes <140/90 mmHg; patients with diabetes <130/80 mmHg). More than 70% of patients on active combination therapy achieved their BP goal by week 24. All combination regimens were well tolerated.
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This was a multicenter, prospective, randomized, double-blind, active-comparator, forced-titration study. After a 3-week placebo run-in, 941 patients were randomized in an 8:1:9 ratio to once-daily treatment with OM (20 mg for 4 weeks, then OM 40 mg for 4 weeks [n = 420]), placebo plus OM (placebo for 2 weeks, then OM 20 mg for 2 weeks and OM 40 mg for 4 weeks [n = 52]), or LOS (50 mg for 4 weeks, then LOS 100 mg for 4 weeks [n = 469]). A subset of 246 patients underwent ambulatory blood pressure (BP) monitoring. The primary endpoint was mean change from baseline in trough seated cuff diastolic BP (SeDBP) at week 8. Secondary endpoints were mean changes from baseline in trough SeDBP at week 4 and seated systolic BP (SeSBP) at weeks 4 and 8. Tertiary endpoints included change from baseline in mean 24-hour ambulatory BP at weeks 4 and 8 and percentage of patients achieving seated cuff BP (SeBP) goal of < 140/90 mm Hg and mean 24-hour ambulatory BP target of < 130/80 mm Hg at weeks 4 and 8.
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A simple, selective, sensitive, precise, simultaneous high performance liquid chromatographic analysis of serum samples and commercial tablet formulation containing hydrochlorothiazide, olmesartan medoxomil and irbesartan are reported. Good chromatographic separation was achieved using a micro-Bondapak, C18 column (15 cm x 4.6 mm, 5 microm), and a mobile phase consisting of acetonitrile-0.2% acetic acid aqueous solution (50:50, v/v) at a flow rate of 1.0 mL/min. The ultraviolet detector was set at a wavelength of 260 nm. Hydrochlorothiazide, olmesartan medoxomil, and irbesartan were eluted at 1.2, 3.8, and 4.4 min, respectively. No extraneous materials were found to interfere. The method uses protein precipitation with acetonitrile for the preparation of serum sample. The linear ranges for hydrochlorothiazide, olmesartan medoxomil, and irbesartan were 6.25-18.75, 20-60, and 75-225 ng/mL, respectively. The recoveries of hydrochlorothiazide, olmesartan medoxomil, and irbesartan in spiked samples were all greater than 98%, and their relative standard deviations were less than 2.0%. The limits of detection were 1, 2, and 2 ng/mL for hydrochlorothiazide, olmesartan medoxomil, and irbesartan, respectively, and the limits of quantification were 3 ng/mL, which allow their determination at the expected serum concentration levels.
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Aortic valve sclerosis (AVS) is a chronic progressive disease involving lipid infiltration, inflammation, and tissue calcification. Despite its high prevalence, there are currently no clinically approved pharmaceuticals for the management of AVS. The objective of the current study was to elucidate the effects of an angiotensin II type 1 receptor blocker, alone or in combination with statin therapy, on the progression of AVS.
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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 pressure.
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We identified hypertensive patients with type 2 DM who had been treated with monotherapy with losartan (n = 214), valsartan (n = 266), telmisartan (n = 185), candesartan (n = 458), or olmesartan (n = 192), in whom laboratory data of SUA between November 1, 2004 and July 31, 2011 were available, from the Nihon University School of Medicine's Clinical Data Warehouse (NUSM's CDW). We used a propensity-score weighting method and a multivariate regression model to adjust for differences in the background among ARB users, and compared the SUA level. The mean exposure of losartan was 264.7 days, valsartan 245.3 days, telmisartan 235.9 days, candesartan 248.9 days, and olmesartan 234.5 days.
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AT1 receptor antagonists such as olmesartan represent a valid therapeutic option for the treatment of hypertension and other cardiovascular and renal diseases.
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Arterial calcification is a common complication of several disorders and is a strong predictor of mortality. The mechanism underlying arterial calcification is not fully understood and as such, no pharmaceutical therapies are currently available which impede its progression. The aim of this study was to investigate the effects of an angiotensin II (AngII) type 1 receptor blocker (ARB) on arterial calcification.
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Combination therapy was required by 159 patients. Changes from baseline in mean 24-hour ambulatory BP (± standard deviation [SD]) were -24.2 (± 11.8)/-11.8 (± 6.9) mmHg, -26.5 (± 11.8)/-12.6 (± 6.7) mmHg, and -24.7 (± 12.5)/-11.2 (± 6.4) mmHg in the stage 1, stage 2, and ISH cohorts, respectively (all p < 0.001 vs baseline). Mean SeBP changes (± SD) from baseline in patients titrated to OM/HCTZ 40 mg/25 mg were -24.6 (± 11.4)/-10.5 (± 7.3) mmHg in the stage 1 cohort, -26.4 (± 17.2)/-11.3 (± 9.7) mmHg in the stage 2 cohort, and -21.5 (± 15.6)/-6.8 (± 7.8) mmHg in the ISH cohort (all p < 0.001). The cumulative proportions of patients achieving an SeBP goal of <140/90 mmHg by week 12 were 88.3%, 56.0%, and 72.4% in the stage 1, stage 2, and ISH cohorts, respectively, while 72.4% of patients achieved an SeSBP of <140 mmHg in the ISH cohort. Treatment-emergent AEs ranged from 32.3% to 32.8%, with <3% of patients reporting drug-related hypotension.
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In a multi-center, prospective study, we investigated the long-term efficacy of olmesartan by ABPM in 18-75 years-old Chinese patients with mild to moderate hypertension (clinic diastolic blood pressure [DBP] 90-109 mm Hg and systolic blood pressure [SBP] < 180 mmHg). After a 1 week placebo runin, 87 patients were treated with olmesartan 20 mg once daily in the morning for 24 weeks. Ambulatory blood pressure monitoring was conducted at baseline and at the end of 24 weeks. At baseline, patients with an MBPS > or = 23 mmHg were classified as the MBPS group (n = 41), and all other patients were classified as the non-MBPS group (n = 46).
In human fibroblasts, HGF significantly increased the production of matrix metalloprotease-1 (MMP-1) and urokinase plasminogen activator, whereas HGF also significantly attenuated the reduction of MMP-1 activity induced by Ang II. In contrast, HGF significantly decreased transforming growth factor (TGF)-beta mRNA stimulated by Ang II, whereas HGF also decreased basal TGF-beta protein level without affecting growth. Similarly, in rat cardiac fibroblasts, HGF inhibited the expression and production of TGF-beta, whereas HGF upregulated its specific receptor, c-met. Conversely, in vivo experiments revealed that administration of temocapril and CS-866 to cardiomyopathic hamsters resulted in a significant decrease in fibrotic area and increase in cardiac HGF concentration and mRNA (P<0.01), whereas cardiac concentration and mRNA of HGF were significantly decreased in cardiomyopathic hamsters. In contrast, mRNA expression of collagen III was markedly decreased by treatment with temocapril and CS-866.
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