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Benicar (Olmesartan)
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Benicar

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:

Similar Products:
Lasix, Norvasc, Toprol, Hyzaar, Teveten, Edarbi, Cozaar, Atacand, Micardis

 

Also known as:  Olmesartan.

Description

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.

Dosage

Take Benicar orally with or without food.

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

Overdose

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

Storage

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.

Contraindications

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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Treatment with CS866 and amlodipine induced a significant reduction of blood pressure in 2K1C-RVH rats. In rats treated with pH 3.5 dialysis solution, necropsy findings revealed features identical to those of encapsulating peritoneal sclerosis (EPS). The typical appearance was multiple surfaces covered with granulation tissue or fibrosic tissue or both. Multiple adhesions were present. Microscopic findings revealed that acidic dialysis solution induced peritoneal fibrosis and loss of mesothelium. Treatment with CS866 prevented the progression of peritoneal fibrosis and adhesions. However amlodipine did not improve the progression of peritoneal fibrosis and peritoneal adhesions. In CS866-treated rats, no signs of EPS were present.

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This 12-week, randomized, double-blind, forced-titration study compared the efficacy of 3 angiotensin receptor blockers. Patients received olmesartan medoxomil 20 mg, losartan potassium 50 mg, valsartan 80 mg, or placebo once daily. At week 4, doses were titrated to 40, 100, and 160 mg once daily for olmesartan, losartan, and valsartan, respectively. At week 8, losartan was increased to 50 mg twice daily and valsartan increased to 320 mg once daily (olmesartan remained at 40 mg once daily). The primary end point was mean change from baseline in seated diastolic blood pressure (SeDBP) at week 8. All 3 medications significantly reduced mean SeDBP from baseline compared with placebo at weeks 4, 8, and 12 (P<.001). At week 8, olmesartan reduced mean SeDBP more than losartan (P<.001); more patients in the olmesartan medoxomil group achieved a blood pressure goal of <140/90 mm Hg (P<.001). Olmesartan did not reduce mean SeDBP significantly compared with valsartan, although more patients attained blood pressure goal with olmesartan (P=.031). At week 12, all agents lowered blood pressure equivalently.

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Olmesartan medoxomil (OM) is one of the newest members of the angiotensin receptor blocker (ARB) family. The renoprotective effects of the angiotensin II type 1 receptor antagonist OM was investigated in a streptozotocin (STZ)-induced diabetic rat model. In this study, we investigated whether OM was able to ameliorate diabetic nephropathy (DN). Thirty male Sprague Dawley rats were assigned to 3 groups: the non-diabetic (group A, n=10), the untreated STZ-induced DN control (group B, n=10) and the STZ-induced DN treated with OM (group C, n=10). Blood pressure (BP) and glucose, creatinine (Cr), blood urea nitrogen (BUN), superoxide dismutase (SOD), malondialdehyde (MDA) microalbumin and urinary protein concentrations were measured. In STZ diabetic rats, BP, glucose, Cr, BUN, MDA and urinary protein levels were significantly increased compared to the non-diabetic control group. OM significantly improved the biological indices in the DN rats. The renal pathological changes were also observed under a light microscope. Our results suggested that OM exerted renoprotective effects on rats with STZ-induced diabetes.

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Serum cholesterol and low density lipoprotein levels were significantly higher in atherosclerosis model group than in control group[(15.08±1.64) vs (2.06±0.15) mmol/L, (15.60±1.05) vs (0.00±0.00) mmol/L] (all P<0.01), while triglyceride level was similar between the two group.In contrast to model group, the mice in intervention group showed no statistical difference in blood pressure and plasma lipid levels, while the plaque areas in the aorta were significantly decreased (P<0.05) as well as the expression of Cat S and Mac-3[(2.4±1.2) vs (8.8±3.2)%, (2.2±1.2) vs (7.2±2.8)%] (all P<0.01). In addition, the elastin levels, collagen contents, and the expression of ASMA remained significantly higher compared with model group (P<0.05).

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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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These results provide a mechanistic rationale for the olmesartan's antioxidant and anti-inflammatory potential translation toward antiatherosclerotic and antiremodeling effects reported on clinical ground.

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This study shows that olmesartan medoxomil, at oral dose of 20 mg-40 mg once daily was effective and safe for hypertension treatment and the hypotensive effect was superior to losartan potassium (50 mg-100 mg once daily).

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It is well recognized that angiotensin II is involved in the pathogenesis of hypertension. Less well recognized - until recently, at least - is its involvement in the pathogenesis of atherosclerosis. However, it is now evident that angiotensin II promotes oxidative stress, vascular remodelling, inflammation, and the formation of atherosclerotic lesions. These actions, which are mediated almost exclusively by the angiotensin II type 1 (AT(1)) receptor, can be blocked by administration of angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]). Of the seven ARBs currently in clinical use, olmesartan is one of the most effective. The rapid and consistent antihypertensive efficacy of this drug, which allows a high proportion of patients to achieve their target blood pressure (BP), is associated with beneficial effects on oxidative stress, vascular remodelling, inflammation, and atherosclerotic lesion formation. These effects appear to be independent of the BP-lowering activity of olmesartan. In clinical trials, olmesartan has been shown to control microinflammation in hypertensive patients, to reduce oxidative stress in patients with type 2 diabetes mellitus, and to normalize the wall: lumen ratio of small resistance arteries (a measure of vascular remodelling) in patients with hypertension. Moreover, in a 2-year study involving hypertensive patients with carotid atherosclerosis (the MORE [Multicentre Olmesartan atherosclerosis Regression Evaluation] trial), olmesartan reduced the intima-media thickness of the carotid artery and significantly reduced the volume of large atherosclerotic plaques. These data suggest that olmesartan may reduce cardiovascular risk by simultaneously normalizing BP and reversing the proatherogenic effects of angiotensin II.

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Olmesartan medoxomil has a favorable safety and efficacy profile, with blood pressure-lowering effects comparable to those of other angiotensin receptor blockers (i.e., losartan, valsartan, irbesartan). At this time, formulary decisions will be driven primarily by economic issues. Theoretical benefits of olmesartan medoxomil in reducing atherogenesis and lowering angiotensin II concentrations better than the alternative agents will be determined only with more extensive research.

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Angiotensin receptor antagonists (angiotensin receptor blockers; ARBs) are an effective initial antihypertensive monotherapy in many patients. However, when initial ARB monotherapy fails to achieve the recommended BP goal, there is some controversy as to whether dose uptitration or the addition of a diuretic is more appropriate. This article addresses this issue by reviewing the dose-response characteristics of olmesartan medoxomil and other ARBs, as well as the relationship between ARB uptitration and BP goal attainment. Two types of trial designs are used to assess dose response: dose-ranging studies (usually a parallel design using different doses across different patient groups), which are used to establish the optimal dose for US FDA registration purposes, and dose-titration studies (increased dosing within the same patients and treating to goal BP). Since dose titration is within the same patient, it may be considered more appropriate for demonstrating dose-response characteristics and demonstration of BP goal attainment. While results from dose-ranging studies suggest that the dose-response curve for some ARBs may be flat, dose-titration studies indicate that significant improvements in BP control and BP goal attainment can be achieved with ARB uptitration. In an integrated analysis of seven US and European randomized, placebo-controlled, dose-ranging trials involving 3055 patients with stage 2 hypertension treated with olmesartan medoxomil 2.5-80 mg/day or placebo for 8 weeks, all olmesartan medoxomil doses were significantly more effective than placebo in lowering the mean DBP and mean SBP (p

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†Adapted and reproduced from the original article published in Drugs 2010; 70 (18): 2439-47.

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This new analysis supports the results of the earlier investigation, in that indapamide SR 1.5 mg/day appeared to be the most effective drug for producing significant reductions in SBP within 8-12 weeks, which is an essential element in optimising cardiovascular prevention among hypertensive patients. The clinical application of these results should take into consideration all the limitations discussed in this analysis.

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In three case histories, patients' sprue-like symptoms improved when olmesartan (Benicar) therapy was withheld.

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Chronic inflammatory processes might be involved in the progression and destabilization of atherosclerotic plaques. Therefore, identification of the mechanism underlying arterial inflammatory function might lead to the development of novel therapeutic strategies. Angiotensin II (AngII) is implicated in atherogenesis by activating the vascular inflammation system, mainly through monocyte chemotaxis. Therefore, we hypothesized that AngII increases plaque size and promotes destabilization of established atheromas by activating the monocyte chemoattractant protein-1 (MCP-1) pathway.

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The Imai rat is a model of spontaneous focal glomerulosclerosis which leads to nephrotic syndrome, hyperlipidemia, hypertension, and progressive renal failure. We evaluated the effects of angiotensin II receptor type 1 (AT-1)blockade, and compared the results with the effects of the administration of hypolipidemic treatment with a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. All treatments were started at 10 weeks of age when the rats were already proteinuric and continued for 6 months when rats were sacrificed.

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A post hoc analysis of changes in seated SBP (SeSBP) levels in patients treated with olmesartan 40 mg plus amlodipine 5 or 10 mg was carried out to investigate the distribution of SeSBP changes produced by this combination. Patients who reached the end of the 52-week study were categorized by size of SeSBP reduction from baseline as follows: 15 to 30 to 45 mmHg.

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The dissolution of the antihypertensive AT1 antagonist olmesartan in methanol generates in situ a new highly bioactive methyl ether analogue via SN1 mechanism involving an intramolecular proton transfer from carboxyl to hydroxyl group. Theoretical calculations confirmed the thermodynamic control preference of methyl ether versus the antagonistic product methyl ester. Α facile synthetic method for olmesartan methyl ether from olmesartan or olmesartan medoxomil is also described. Interestingly, the introduction of the methyl group to olmesartan did not alter its pharmacological properties. This observation opens new avenues in the synthesis of novel drugs, since hydroxyl and carboxylate groups have an orthogonal relationship in many drugs.

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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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Many patients with hypertension require more than one drug to control their blood pressure.1 Tribenzor (Daiichi Sankyo), recently approved by the FDA for treatment of hypertension, combines the calcium channel blocker amlodipine (Norvasc, and others), the angiotensin receptor blocker (ARB) olmesartan (Benicar) and the most commonly prescribed diuretic, hydrochlorothiazide (HCTZ). Tribenzor is not approved for initial therapy, but is recommended for patients not adequately controlled on any 2-drug combination of a calcium channel blocker, an ARB or a diuretic.

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Pharmacokinetic parameters were evaluated in 6 male and 6 female healthy volunteers (mean age, 22 [range, 20-25] years]; weight, 56.0 [range, 51.0-60.0] kg). Probenecid coadministration increased olmesartan Css-av, AUC0→∞, and AUC0-48 by 40%, 50%, and 50%, respectively (P = 0.018, 0.000, 0.000, respectively), but there was no statistical significance for Tmax, t1/2, Css-max, and Css-min between olmesartan plus probenecid and olmesartan alone (P = 0.697, 0.053, 0.521, and 0.734, respectively). No serious adverse event (AE) was reported during the study. The proportion of volunteers with AEs in the olmesartan plus probenecid period (5 of 12 [42%]) was higher than that in the olmesartan-alone period (1 of 12 [8%]). All of the AEs during the olmesartan plus probenecid period were abnormal routine urine test results. The AE in olmesartan-alone period was dizziness. All AEs were classified as mild and considered to be at least possibly related to treatment. All volunteers recovered from the AEs by 2 weeks after the end of the study.

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Olmesartan medoxomil produced statistically significant reductions from baseline in both systolic and diastolic office BP and BPSM values. In contrast to office BP, telemonitoring of BPSM allowed the early identification of responders (e.g., after 2-3 weeks' treatment). Blood pressure reduction with olmesartan medoxomil was greater for office BP than for BPSM values. Normalization of BP was achieved in 64.2% of the patients using office BP measurement compared with 36.4% using BPSM. Blood pressure self-measurement showed no significant difference between morning and evening BP measurements or between the morning : evening BP ratio at baseline and after nine weeks of olmesartan medoxomil treatment. Compliance and tolerability were good or very good in most patients.

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This study showed that OLM/AML/HCTZ reduced blood pressure and significantly increased blood pressure control whilst improving patients' HRQoL. Achieving blood pressure control, amount of concomitant medication and dosage strength of antihypertensive impacted on patients' HRQoL.

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buy benicar 2016-08-10

Azilsartan medoxomil is a buy benicar safe and effective ARB with a unique pharmacologic profile versus other agents, including slowed angiotensin II type 1 receptor dissociation rates and improved receptor specificity. Studies have shown azilsartan medoxomil 80 mg once daily to reduce BP to a greater extent than valsartan and olmesartan, with similar safety and tolerability.

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To determine the mechanistic similarities of OAE buy benicar with coeliac sprue.

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Uncontrolled blood pressure (BP) remains a leading contributor to cardiovascular disease and mortality worldwide. Although current practice guidelines recommend treating patients with hypertension to defined BP goals, the approach is not widely implemented, and BP control in clinical practice is much worse Anafranil Drug Insert than that attained in clinical trials. Recent and ongoing clinical trials are utilizing more aggressive approaches with combination therapy as initial treatment. This article discusses the problem of therapeutic or clinical inertia when attempting to control hypertension and highlights differences in BP control rates between clinical trials and real-world practice. Additionally, the rationale for an ongoing treat-to-goal study using a fixed-dose combination of amlodipine/olmesartan medoxomil in patients with hypertension not controlled on monotherapy is provided.

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In this multicenter, randomized, double-blind, parallel-group study, Korean patients aged 20 Arcoxia 30 Mg to 75 years with stage 2 hypertension who had a mean seated diastolic blood pressure (msDBP) ≥100 mmHg were enrolled when their BP was uncontrolled [mean seated systolic BP (msSBP)/msDBP >140/90 mmHg or msSBP/msDBP >130/80 mmHg with diabetes or chronic kidney disease] with 4-week dual FDC therapy (OM/HCTZ 20/12.5). The patients were randomized to receive either OM/AML/HCTZ 20/5/12.5 or OM/HCTZ 20/12.5 once daily for 8 weeks. At the end of 8 weeks, patients with uncontrolled BP were assigned to receive either OM/AML/HCTZ 40/5/12.5 or OM/AML/HCTZ 20/5/12.5 in an additional 8-week open-label extension period.

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We report the case of a 63-year-old man presenting with recurrent secretory diarrhoea, acute renal failure and metabolic acidosis. Initial work-up revealed total villous atrophy (Marsh stage IIIC) with intraepithelial lymphocytosis. A gluten-free diet did not have any effect on the diarrhoea. During several periods of hospitalization antihypertensive medications were temporarily stopped due Feldene 10 Mg Tablets to dehydration; this resulted in reduction of his symptoms. Eventually an association between the enteropathy and the antihypertensive olmesartan was suspected. Indeed, permanent withdrawal of olmesartan resulted in permanent clinical improvement.

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BACKGROUNDS AND METHODS: A higher degree of clinical efficacy with olmesartan compared with other angiotensin receptor blockers, has been reported by several sources. In this study of 31 examples of cases of essential hypertension, Glucophage 500 Mg Holter electrocardiogram, ambulatory blood pressure monitoring and pulse wave velocity (PWV) measurements were performed before and after substituting olmesartan 20 mg for candesartan 8 mg antihypertensive drug therapy.

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Adefovir dipivoxil, Alemtuzumab, Aliskiren fumarate, AMA1-C1/alhydrogel, Amlodipine besylate/atorvastatin calcium, Aripiprazole, Artesunate/amodiaquine, Asenapine maleate; Bosentan, Brivaracetam; Carisbamate, Clevudine, Clofarabine, Corticorelin acetate; Dasatinib; Elinogrel potassium, Entecavir, Erlotinib hydrochloride, Eslicarbazepine acetate, Etazolate; Fampridine, Fluarix, Fondaparinux sodium, Fulvestrant; Gabapentin enacarbil, GDC-0941, GI-5005, Golimumab; Imatinib mesylate, Lacosamide, Lapatinib ditosylate, Levetiracetam, Liraglutide, LOLA; Mecasermin, Morphine hydrochloride; Natalizumab, Nilotinib hydrochloride monohydrate; Olmesartan medoxomil, Omacetaxine mepesuccinate; Paclitaxel-eluting stent, Peginterferon alfa-2a, Peginterferon alfa-2b, Pemetrexed disodium, Poly I:CLC, Pralatrexate, Pregabalin; Ranolazine, Rasagiline mesilate, Retigabine hydrochloride, Rhenium Re-186 etidronate, Rosuvastatin calcium, Rotigotine, RTL-1000, Rufinamide; Sirolimus-eluting coronary stent, Sirolimus-eluting stent, Sorafenib, Stiripentol Accutane 10 Mg Day ; Tiotropium bromide; Valsartan/amlodipine besylate, Varenicline tartrate; XL-184; Zoledronic acid monohydrate.

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In this analysis, we evaluated the efficacy of the angiotensin II receptor blocker olmesartan medoxomil in reducing systolic blood pressure (SBP) and pulse Cold Sores And Valtrex Dosage pressure (PP) in hypertensive patients.

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Patients adhering to the instructions for BPSM (at least two measurements daily) had a better response to antihypertensive Norvasc 5mg Medication treatment with olmesartan medoxomil. Whether BPSM per se resulted in an improved adherence to therapy or whether the number of recordings was an indicator of already existing adherence remains to be determined. Obtaining at least five home BP readings per week was identified as the threshold for correctly predicting response to olmesartan medoxomil treatment.

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Olmesartan medoxomil (OM) is a prodrug-type angiotensin II type 1 receptor antagonist. OM is rapidly converted into its active metabolite olmesartan by multiple hydrolases in humans, and we recently identified carboxymethylenebutenolidase homolog (CMBL) as one of the OM bioactivating hydrolases. In the present study, we further investigated the interindividual variability of mRNA and protein expression of CMBL and OM-hydrolase activity using 40 individual human liver and 30 intestinal specimens. In the intestinal samples, OM-hydrolase activity strongly correlated with the CMBL protein expression, clearly indicating that CMBL is a major contributor to the prodrug bioactivation in human intestine. The protein and activity were highly distributed in the proximal region (duodenum and jejunum) and decreased to the distal region of the intestine. Although there was high interindividual variability (16-fold) in both the protein and activity in the intestinal segments from the duodenum to colon Antabuse Injection Cost , the interindividual variability in the duodenum and jejunum was relatively small (3.0- and 2.4-fold, respectively). In the liver samples, the interindividual variability in the protein and activity was 4.1- and 6.8-fold, respectively. No sex differences in the protein and activity were shown in the human liver or intestine. A genetically engineered Y155C mutant of CMBL, which was caused by a single nucleotide polymorphism rs35489000, showed significantly lower OM-hydrolase activity than the wild-type protein although no minor allele was genotyped in the 40 individual liver specimens.

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Animals treated with a combination of the two drugs had hemodynamics, heart weights and dimensions similar to the other treated animals. However, the combination of the two drugs suppressed ANP, BNP and Paracetamol Suppository Paediatric Dose other gene expressions related to contractile proteins of fetal type and collagens more effectively than ACE inhibitor or ARB alone.

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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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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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Intensive blood pressure control is a desirable and obtainable goal in patients with hypertension, according to the most recent treatment guidelines from Europe and the US. Achieving target blood pressure depends on the efficacy of antihypertensive treatment and patient compliance. Olmesartan medoxomil, a non-peptidergic angiotensin AT1 receptor antagonist, has been shown to be effective and well tolerated. Continuation of initial treatment is higher with AT1 receptor antagonists than for any other class of antihypertensive drugs. Olmesartan medoxomil may also have end-organ protective effects that provide additional clinical benefit. Optimal blood pressure control may be achieved faster if initial treatment contains the most efficacious and well tolerated antihypertensive drug or drugs. The ongoing European study, known as OLMEBEST (Efficacy and safety of OLMEsartan: reduction of Blood pressure in the treatment of patients suffering from mild to moderate ESsenTial hypertension), will provide important information on the use of olmesartan medoxomil as an initial treatment for hypertension.

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The impact of SLCO1B1 polymorphism on the pharmacokinetics of olmesartan and on the pharmacokinetic interaction between pravastatin and olmesartan was investigated. On day 1, ten healthy volunteers took an oral dose (10 mg) of pravastatin. After a 3-day washout period, each subject received olmesartan medoxomil (10 mg) for 3 days. On day 8, they received olmesartan medoxomil (10 mg) and pravastatin (10 mg) concurrently, and pharmacokinetic profiles were compared with those in each single-dose phase with regard to the SLCO1B1 genotypes (*1b/*1b, *1b/*15, and *15/*15). In the single-dose phase, the mean C (max) and AUC(0-24) of olmesartan tended to be higher in *15/*15 subjects than in *1b/*1b subjects, while the mean CL( t )/F (+/-SD) in *15/*15 subjects was significantly lower than that in *1b/*1b subjects. No statistically significant differences were observed in any pharmacokinetic parameters between single-dose and co-administration phases for both pravastatin and RMS-416. These results suggest that OATP1B1 plays a role in the pharmacokinetics of olmesartan, and the co-administration of olmesartan does not affect the pharmacokinetics of pravastatin or its metabolite, RMS-416, although larger scale clinical studies are needed to confirm these observations due to the small sample size in the present study.

buy benicar 2015-10-14

We previously reported that α- and β-blockers protected against emotional stress-induced cardiac dysfunction, but the protective effects of other antihypertensive drugs is unknown. The purpose of this study is to evaluate the ability of a calcium channel blocker, amlodipine, to prevent temporal left ventricular hypokinesia after emotional stress compared with an angiotensin II receptor blocker, olmesartan medoxomil.

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After placebo run-in, 192 patients received OM 20 mg/day for 3 weeks. If blood pressure (BP) remained ≥120/70 mmHg, patients were uptitrated every 3 weeks to OM 40 mg/day, OM/HCTZ 40/12.5 mg/day, and OM/HCTZ 40/25 mg/day. Efficacy was evaluated by 24-hour ambulatory BP monitoring. Secondary endpoints included changes in ambulatory systolic BP (SBP) and diastolic BP (DBP) during daytime (08:00 to 16:00) and nighttime (22:00 to 06:00), as well as achievement of prespecified ambulatory BP targets in the total cohort and subgroups based on gender, race, hypertension severity, and age (≥65 or <65 years). Dipper status (nocturnal decrease in BP ≥10% of mean daytime BP) was assessed.

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PubMed, Embase, and Cochrane Library were searched using search terms " azilsartan", "chlorthalidone," "pharmacology," "pharmacokinetics," "pharmacodynamics," "pharmacoeconomics," and "cost-effectiveness." To obtain other relevant information, US Food and Drug Association as well as manufacturer prescribing information were also reviewed.

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Azilsartan, an angiotensin II type 1 (AT(1)) receptor blocker (ARB), was recently approved by regulatory authorities for treatment of hypertension and is the 8th ARB to join the clinical market. This article discusses the medical reasons for introducing a new AT(1) receptor blocker and reviews the experimental and clinical studies that have compared the functional properties of azilsartan to those of other ARBs. The main question addressed is: Does azilsartan have distinguishing features that should motivate choosing it over any of the other sartans for use in clinical practice? Based on studies conducted to date in hypertensive patients without serious comorbidities, azilsartan appears to be characterized by a superior ability to control 24-hour systolic blood pressure (BP) relative to other widely used ARBs including valsartan, olmesartan, and candesartan, and presumably others as well (eg, losartan). Compared to these other ARBs, azilsartan may increase the BP target control and response rate by an absolute value of 8%-10%. Greater antihypertensive effects of azilsartan might be due in part to its unusually potent and persistent ability to inhibit binding of angiotensin II to AT(1) receptors. Preclinical studies have indicated that azilsartan may also have potentially beneficial effects on cellular mechanisms of cardiometabolic disease and insulin sensitizing activity that could involve more than just blockade of AT(1) receptors and/or reduction in BP. However, the clinical relevance of these additional actions is unknown. Given that the general ability of antihypertensive drugs to protect against target organ damage is largely mediated by their ability to decrease BP, the enhanced antihypertensive effects of azilsartan should serve to justify clinical interest in this ARB relative to other molecules in the class that have a lower capacity to reduce BP.

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Although chronic cardiac dysfunction is known to progressively exacerbate renal injury, a condition known as type 2 cardiorenal syndrome (CRS), the mechanism responsible is largely unknown. The present study was undertaken to clarify the mechanism of renal injury in rats with both unilateral nephrectomy (NX) and surgically induced myocardial infarction (MI), corresponding to a model of type 2 CRS. Compared with a control group, rats with both MI and NX (MI+NX) exhibited progressive proteinuria during the experimental period (34 wk after MI surgery), whereas proteinuria was not observed in rats with MI alone and was moderate in rats with NX alone. The proteinuria in rats with MI+NX was associated with renal lesions such as glomerulosclerosis and infiltration of mononuclear cells and upregulation of the renal proinflammatory and -fibrotic cytokine and angiotensin II type 1a receptor (AT1aR) genes. In contrast, plasma renin activity was lowered in rats with MI+NX. Immunohistochemistry revealed that the increased AT1R protein was present mainly in renal interstitial mononuclear cells. Olmesartan medoxomil, an AT1R blocker, markedly reduced the proteinuria and infiltration of mononuclear cells, whereas spironolactone, a mineralocorticoid receptor blocker, did not. The present findings demonstrate the pathogenetic role of renal interstitial AT1R signaling in a model of type 2 CRS, providing evidence that AT1R blockade can be a useful therapeutic option for this syndrome.

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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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Diabetic nephropathy (DN) is a leading cause of endstage renal disease (ESRD) in Japan and Hong Kong. Asian patients are known to be more predisposed to DN and ESRD than Caucasians. Strict blood glucose and blood pressure control are key factors in prevention and treatment of DN. In the last decade, inhibition of the renin-angiotensin-aldosterone (RAA) system has been confirmed to reduce the incidence of cardiovascular complications in Caucasian patients with diabetes. Although the RENAAL study has demonstrated the beneficial effects of inhibition of the RAA system on prevention of ESRD and death in type 2 diabetic patients with overt proteinuria, only 17% of patients in this multicenter study were of Asian ethnicity. Given the predilection of Asian diabetic patients for renal complications and the rising burden of ESRD, there is a need to confirm these findings in a homogenous group of Asian patients. The ORIENT (Omesartan Reducing Incidence of Endstage Renal Disease in Diabetic Nephropathy Trial) is a randomized, double-blind, placebo-controlled study in Japan and Hong Kong to evaluate the renal protective benefits of olmesartan medoxomil in type 2 diabetic patients with overt proteinuria (urinary albumin to creatinine ratio > or =300 mg/g creatinine) and renal insufficiency (serum creatinine: 1.0-2.5 mg/dl). The study has a targeted enrollment of 400 Japanese and Hong Kong Chinese patients. The primary outcome is the composite endpoint of time to the first occurrence of doubling of serum creatinine, ESRD (serum creatinine more than 5.0 mg/dl, the need for chronic dialysis, or renal transplantation) or death. The average follow-up period is 4 years and the study ends in 2009.

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BP-CRUSH (Blood Pressure Control in All Subgroups With Hypertension) was a phase IV, prospective, open-label, multicenter, single-arm, dose-titration study (N = 999). The present subgroup analysis reports the efficacy/safety of up to 20 weeks of treatment with amlodipine (AML)/olmesartan medoxomil (OM) ± hydrochlorothiazide (HCTZ) in obese and non-obese patients with hypertension uncontrolled on antihypertensive monotherapy.

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The distributions of olmesartan medoxomil and hydrochlorothiazide were best fitted using a two-compartment model with no lag time and first-order elimination. When analyzing hydrochlorothiazide kinetics, we found that TCHO and CL/F were correlated, while. HB and Ka influenced olmesartan medoxomil modeling. All evaluations indicated that the pharmacokinetic profiles of olmesartan medoxomil and hydrochlorothiazide were adequately described using our PPK model.

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Vascular injury was induced by polyethylene cuff-placement around the mouse femoral artery. Some mice were treated with AT1 receptor blocker, olmesartan, at the dose of 3 mg.kg(-1).day(-1) with an osmotic minipump. Neointima formation and the proliferation of vascular smooth muscle cells (VSMCs) were measured by morphometric analysis and bromodeoxyuridine (BrdU) incorporation. MCP-1 and TNF-alpha expression was detected by Western blot and immunohistochemical staining.

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Angiotensin II is a vasoactive hormone of the renin-angiotensin system and plays an important role in the pathophysiology of several organ damages. Angiotensin II receptor blockers have been shown to be effective in treating both hypertension and connected organ damages. It is well known that although the angiotensin II receptor blockers have structural and pharmacokinetic differences, few pharmacological differences separate them. One of these is the degree of binding to the angiotensin II receptor type 1 compared with the angiotensin II receptor type 2; olmesartan medoxomil exhibits more than a 12,500-fold greater affinity for the angiotensin II receptor type 1 receptor than for the angiotensin II receptor type 2, making it theoretically the second most potent agent. However, olmesartan's excellent receptor interaction is based on the combination of several specific pharmacokinetic factors. Potential advantages of this drug include once-daily dosing, a very low incidence of significant adverse reactions and/or events and a well-tolerated side effect profile. Nowadays, we have a lot of information about the pharmacology, antihypertensive efficacy and safety of olmesartan medoxomil, to further extend many clinical studies are still continuing to evaluate the potential benefits of high dosages and/or combination of this molecule.

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Probenecid increases the exposure speed of olmesartan by increasing the AUC0-48, AUC0→∞, and Css-av. The combined treatment of olmesartan medoxomil with probenecid may increase the occurrence of genitourinary side effects. ClinicalTrials.gov identifier: NCT01907373.

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To review pharmacology and clinical role of AZI monotherapy and AZI/CLT or AZI/amlodipine combination therapies for hypertension management.