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Cozaar

Cozaar is an effective medication which helps to fight with the symptoms of high blood pressure and to reduce the risk of stroke in people with hypertension. It is used in the treatment of kidney problems in people with type 2 diabetes. Cozaar acts by preventing the hormone angiotensin II from constricting the blood vessels, which tends to raise blood pressure.

Other names for this medication:

Similar Products:
Lasix, Norvasc, Toprol, Hyzaar

 

Also known as:  Losartan.

Description

Cozaar is a perfect remedy, which helps to fight against the symptoms of high blood pressure and to reduce the risk of stroke in people with hypertension.

Its target is to treat kidney problems in people with type 2 diabetes.

Cozaar is also known as Losartan potassium, Cosart, Los-Po.

Cozaar acts by preventing the hormone angiotensin II from constricting the blood vessels, which tends to raise blood pressure. It is angiotensin II receptor antagonists.

Generic name of Cozaar is Losartan Potassium.

Brand name of Cozaar is Cozaar.

Dosage

Take Cozaar tablets orally with or without food.

Do not crush or chew it.

Take Cozaar once or twice a day at the same time.

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

Overdose

If you overdose Cozaar and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Cozaar overdosage: fainting, feeling lightheaded, rapid heartbeat.

Storage

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

Side effects

The most common side effects associated with Cozaar 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 Cozaar if you are allergic to Cozaar components.

Do not take Cozaar if you're pregnant or you plan to have a baby, or you are a nursing mother. Cozaar can harm your baby.

Do not use Cozaar if you are taking salt substitutes or potassium supplements, other blood pressure medicine, diuretic (water pill).

It can be dangerous to use Cozaar if you suffer from or have a history of liver disease, kidney disease, heart failure.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Avoid machine driving.

Do not stop taking Cozaar suddenly.

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Induction of diabetes led to significant increase in retinal expression of prorenin but not the (pro)renin receptor. Retinal adherent leukocytes were significantly suppressed with PRRB. Administration of PRRB inhibited diabetes-induced retinal expression of VEGF and ICAM-1. To clarify the role of signal transduction via the (pro)renin receptor in the diabetic retina, we used AT1-R-deficient mice in which the RAS was deactivated. Retinal adherent leukocytes in AT1-R-deficient diabetic mice were significantly suppressed with PRRB. PRRB suppressed the activation of ERK and the production of VEGF, but not ICAM-1, in AT1-R-deficient diabetic mice.

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AT1R and AT2R levels did not differ between BS/GS and healthy controls. Ang II induced ERK1/2 phosphorylation in BS/GS fibroblasts, but peak ERK1/2 phosphorylation declined more rapidly than that in control and BS/GS fibroblasts also exhibited increased MKP-1 levels at 30-min incubation. PD123319, an AT2R blocker in BS/GS fibroblasts, abolished the increased MKP-1 and ERK1/2 phosphorylation time course became same as that for control. Losartan, an AT1R blocker, alone altered the time course of control fibroblast MKP-1 to mimic the increase seen in BS/GS fibroblasts, whereas ERK1/2 declined concomitantly. Treatment with Losartan and PD123319 in controls reduced MKP-1 and elevated ERK1/2 phosphorylation to the level observed in BS/GS patients treated with PD123319.

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To evaluate the efficiency and safety of two treatment regimens using ramipril or losartan in combination with hydrochlorothiazide (HCT) and amlodipine in grade 1-2 arterial hypertension (AH).

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Thirty male Sprague-Dawley rats were randomly divided into Control group, ALI group (LPS), and Losartan group (LPS + Losartan). Bronchoalveolar lavage fluid (BALF) and lung tissue were obtained for analysis. The expressions of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), intercellular adhesion molecule-1 (ICAM-1) and caspase-3 were detected by reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting.

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In guinea pigs with descending aortic banding, treatment with losartan for 8 weeks neither attenuates progression of pressure overload hypertrophy nor significantly improves impaired mass-normalized pressure-derived indices of LV contraction and relaxation.

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The findings of LAARS, the first large study with an AII antagonist that examined IMT, suggest that AII antagonism reverses the early stages of vascular hypertrophy in patients with hypertension. Further studies are needed to delineate the relative importance of AII antagonism versus blood pressure reduction per se in mediating the beneficial vascular effects of losartan.

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Losartan is an angiotensin II receptor antagonist that is metabolized by CYP2C9 and CYP3A4 to a more potent antihypertensive metabolite, E3174. Interaction studies with inhibitors of CYP3A4 have not demonstrated significant changes in the pharmacokinetics of losartan or E3174. The authors assessed the steady-state pharmacokinetics of losartan and E3174 when administered alone and concomitantly with fluvastatin, a specific CYP2C9 inhibitor. A prospective, open-label, crossover study was conducted in 12 healthy volunteers with losartan alone and in combination with fluvastatin. The baseline phase was 7 days of losartan (50 mg QAM), and the inhibition phase was 14 total days of fluvastatin (40 mg QHS), with the final 7 days including losartan. The authors found that fluvastatin did not significantly change the steady-state AUC0-24 or half-life of losartan or E3174. Losartan apparent oral clearance was not affected by fluvastatin. Inhibition of losartan metabolism appears to require both CYP2C9 and CYP3A4 inhibition.

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To observe the effects of different concentrations Angiotensin II on the transcription of LOX1 in culture human umbilical vein endothelial cells and to explore its mechanism.

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Treatment with losartan causes an increase in urinary Zn excretion and induces Zn deficiency in patients with hypertension. The addition of hydrochlorothiazide has an additive effect. Magnesium and nitric oxide metabolism are not affected by either treatment.

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The contribution of brain angiotensin II (ANG II) to thirst and Na+ appetite of sheep was evaluated. Thirst was stimulated by water deprivation, intracarotid or intracerebroventricular infusion of ANG II, or intracarotid or intracerebroventricular infusion of hypertonic solution. Intracerebroventricular infusion, over 1-3 h, of the ANG II type 1 (AT1) receptor antagonist, losartan, decreased or abolished water intake caused by all of the stimuli tested. Intracerebroventricular infusion of ZD-7155, another AT1-receptor antagonist, blocked ANG II-induced water intake. Neither losartan nor ZD-7155 infused intracerebroventricularly altered the Na+ appetite of Na(+)-depleted sheep. Intracerebroventricular infusion of losartan over 3 h, however, did block the increase in water intake and the decrease in Na+ intake caused by intracerebroventricular infusion of hypertonic NaCl in Na(+)-depleted sheep. Intracerebroventricular infusion of the ANG II type 2 (AT2) receptor antagonist, PD-123319, over 1-3 h, did not alter ANG II-induced water intake or Na+ depletion-induced Na+ intake. These results are consistent with the proposition that brain ANG II, working via AT1 receptors, is involved in the neural system controlling some aspects of physiological thirst and Na+ appetite. A role for AT2 receptors in physiological thirst or Na+ appetite is not supported by the present results.

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The ELITE II study will further define the role of losartan in the treatment of patients with symptomatic heart failure relative to the angiotensin-converting enzyme inhibitor captopril, an agent from a class currently considered standard treatment for this disease.

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The aim of the study was to compare the effects of long-term treatment with different types of antihypertensive drugs on left ventricular hypertrophy (LVH) and diastolic function in patients with essential hypertension. We examined 60 patients with mild to moderate hypertension from 35 to 55 years old (middle age 44.3 +/- 2.3 yrs) having no concomitant diseases. Patients were treated for six months with different types of antihypertensive drugs: 21 patient received nifedipine-retard 40 mg/day, 20--atenolol 100 mg/day, 10--losartan potassium 100 mg/day, 9--perindopril 4 mg/day. Cardiac structure and function was studied by echocardiography. For the left ventricle (LV) the diastolic mass normalised for body surface area (LVMI), the ratio of the early and atrial mitral inflow velocities (E/A), isovolumetric relaxation time (IVRT), relative wall thickness (RWT) were measured. After six months of treatment LVMI decreased by 9% in nifedipine group (P < 0.01), by 10.5% in atenolol group (P < 0.01), by 12% in losartan group (P < 0.01) and by 8.2% in perindopril group (NS). RWT decreased in all groups, while diastolic dimension index remained unchanged. The reversal of LVH was not related to blood pressure reduction. It was more significant in patients with initially higher values of LVMI. Antihypertensive effects of the drugs were comparable. Long-term treatment with all types of selected drugs improves cardiac structure and function independently of their antihypertensive action. Our data suggest that on the basis of the influence on cardiac remodelling no preference for any studied drug can be discerned. The work had the following source of support: the atenolol (Falitonsin) and nifedipine-retard (Corinfar-retard) were provided by the AWD Company (Germany), losartan potassium has been provided by Merck Sharp & Dohme Company and perindopril (Prestarium) by the Servier Group.

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A total of 237 eligible patients with mean trough sitting diastolic blood pressure (SiDBP) 95-115 mmHg and a mean trough sitting systolic blood pressure (SiSBP) < 190 mmHg entered the baseline period of treatment with valsartan 80 mg/day for 4 weeks. Those (n = 165) whose SiDBP remained > 90 mmHg and who were not excluded for other reasons were then switched to a single-tablet formulation of losartan 50 mg/hydrochlorothiazide 12.5 mg combination once daily for a further 4 weeks.

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CATH.a cells were incubated with Ang II in combination with mitochondrial permeability transition pore (mPTP) inhibitors or angiotensin receptor antagonists, and apoptosis rate, caspase-3 activity, cytochrome c levels, and mPTP opening were assessed.

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White-coat hypertension (HT) and masked HT can be identified by home blood pressure (BP) measurement. The prevalence of these subtypes and the associated risk of cardiovascular disease have not been fully investigated among Japanese hypertensive patients. The risk of cardiovascular events due to HT and its relationship with home BP measurement were examined among Japanese hypertensive patients receiving treatment in the Japan Hypertension Evaluation with Angiotensin II Antagonist Losartan Therapy (J-HEALTH) study, a nationwide prospective observational study. Both home and clinic BP were measured during treatment, and the occurrence of cardiovascular events was monitored in 4,596 Japanese patients (mean age of 60.8 years, 43.2% men, and mean follow-up period of 3.5 years). HT was defined as a systolic BP > or =140 mmHg for clinic BP and > or =135 mmHg for home BP while on treatment. The relative risk of all cardiovascular events and stroke increased along with higher clinic and home BP levels during treatment. The prevalence of white-coat HT, masked HT, well-controlled HT, and poorly controlled HT was 12.6%, 19.5%, 23.8%, and 44.1%, respectively. The relative risk of cardiovascular events was not significantly increased in the poorly controlled HT (relative risk [RR]: 2.05, 95% confidence interval [CI]: 0.77-5.45), white-coat HT (RR: 0.77, 95% CI: 0.15-3.96), and masked HT (RR: 2.00, 95% CI: 0.67-5.98) subgroups compared with the well-controlled-HT subgroup; however, the risk of masked HT was similar to that of poorly controlled HT. Monitoring both clinic and home BP is important to diagnose masked HT and to prevent cardiovascular disease in this subtype of HT. However, further investigation is required to fully characterize the cardiovascular risks associated with masked HT among Japanese patients receiving treatment.

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Mutations in sarcomere protein genes can cause hypertrophic cardiomyopathy (HCM), a disorder characterized by myocyte enlargement, fibrosis, and impaired ventricular relaxation. Here, we demonstrate that sarcomere protein gene mutations activate proliferative and profibrotic signals in non-myocyte cells to produce pathologic remodeling in HCM. Gene expression analyses of non-myocyte cells isolated from HCM mouse hearts showed increased levels of RNAs encoding cell-cycle proteins, Tgf-β, periostin, and other profibrotic proteins. Markedly increased BrdU labeling, Ki67 antigen expression, and periostin immunohistochemistry in the fibrotic regions of HCM hearts confirmed the transcriptional profiling data. Genetic ablation of periostin in HCM mice reduced but did not extinguish non-myocyte proliferation and fibrosis. In contrast, administration of Tgf-β-neutralizing antibodies abrogated non-myocyte proliferation and fibrosis. Chronic administration of the angiotensin II type 1 receptor antagonist losartan to mutation-positive, hypertrophy-negative (prehypertrophic) mice prevented the emergence of hypertrophy, non-myocyte proliferation, and fibrosis. Losartan treatment did not reverse pathologic remodeling of established HCM but did reduce non-myocyte proliferation. These data define non-myocyte activation of Tgf-β signaling as a pivotal mechanism for increased fibrosis in HCM and a potentially important factor contributing to diastolic dysfunction and heart failure. Preemptive pharmacologic inhibition of Tgf-β signals warrants study in human patients with sarcomere gene mutations.

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Syndrome differentiation-based TCM treatment in addition to basic treatments can produce satisfactory therapeutic effects on proteinuria in patients with chronic kidney disease by improving the clinical symptoms, reducing TCM symptom scores and proteinuria, and protecting the renal functions.

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Angiotensin II (Ang II) plays an important role in cardiac remodeling through stimulation of proliferation and extracellular matrix (ECM) production in cardiac fibroblasts. Integrins are a family of transmembrane receptors that mediate the attachment of cells to ECM. We hypothesized that Ang II regulation of integrins further contributes to its role in cardiac remodeling. We cultured adult rat cardiac fibroblasts with and without Ang II (100 nmol/L) to determine the effects on mRNA and protein levels of integrins, as well as alpha-actinin and other cytoskeletal proteins that link to integrins at the site of focal adhesions. Ang II was also added in the presence of irbesartan (10 micromol/L), a specific Ang II type 1 (AT(1)) receptor antagonist, or PD 123319 (10 micromol/L), a specific Ang II type 2 receptor antagonist. To investigate the function of these integrins, we determined the effects of blocking antibodies on Ang II-induced adhesion to ECM. We also treated spontaneously hypertensive rats (SHR) with an AT(1) receptor blocker, losartan, or with hydralazine to investigate integrin and alpha-actinin expression in treated and untreated SHR. Ang II enhanced alpha(v), beta(1), beta(3), and beta(5) integrins; osteopontin; and alpha-actinin mRNA and protein levels in cardiac fibroblasts. All of these effects were inhibited by irbesartan but not by PD 123319. Pretreatment of cardiac fibroblasts with Ang II enhanced cell attachment to ECM proteins and induced focal adhesion kinase phosphorylation. Blocking antibodies to beta(3) and alpha(v)beta(5) attenuated Ang II-induced adhesion. In SHR, ventricular alpha(v) and beta(5) integrin expression and alpha-actinin were increased compared with those in Wistar-Kyoto rats. Although both losartan and hydralazine lowered mean arterial pressure and decreased peripheral vascular resistance, only losartan attenuated the increased integrin, alpha-actinin, fibronectin laminin, and osteopontin expression and the increased left ventricular mass (as determined with echocardiography). Hydralzine had none of these effects. Although both agents attenuated beta-myosin heavy chain expression, a marker of hypertrophy, losartan had a greater effect. These results suggest that integrins and alpha-actinin are upregulated by Ang II and in left ventricular hypertrophy and that the block of expression of these proteins through inhibition of the AT(1) receptor is associated with attenuation of the hypertrophic response. Ang II induces integrin and alpha-actinin expression in cardiac fibroblasts that is associated with adhesion and left ventricular hypertrophy and blocked through inhibition of the AT(1) receptor.

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To compare angiotensin receptor blocker utilization and expenditure patterns in Austria and Croatia following prescribing restrictions, as well as with other European countries introducing different supply- and demand-side measures. Lastly, to appraise the impact of generic losartan in Croatia on utilization of patented angiotensin receptor blockers.

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To assess the efficacy of losartan (2-n-butyl-4-chloro-5-hydroxymethyl-1-[(2'-(1H-tetrazol-5-yl)biphe nyl-4-yl)methyl]imidazole, potassium salt), an angiotensin II receptor antagonist, on acute myocardial ischemia, 36 four-month-old spontaneously hypertensive rats were used. The animals underwent 45 min of left coronary artery occlusion and 1 h of reperfusion and were randomly assigned to control and losartan-treated groups (2, 5, and 10 mg/kg, intravenously). Losartan was administered 15 min before ischemia. Electrocardiograms (lead II) were monitored continuously throughout the experiment. To assess the anti-infarct effect of losartan, the area at risk was determined by methylene blue dye and the infarct size was determined by nitroblue tetrazolium chloride staining. The areas of risk and infarct were measured by computerized planimetry. Results demonstrated that the low and intermediate doses (2 and 5 mg/kg) of losartan significantly decreased the incidence of ventricular fibrillation and mortality during the ischemic period induced by left coronary artery occlusion. However, a significant reduction in infarct size, calculated as a percentage of the area at risk, was noted in all three losartan-treated groups (control: 41.5% +/- 5.2%, losartan, 2 mg/kg: 11.2% +/- 5.8%, 5 mg/kg: 8.5% +/- 2.7% and 10 mg/kg: 13.7% +/- 1.6%). The results suggest that losartan may be useful in the treatment of ventricular arrhythmias induced by acute myocardial infarction and attenuation of reperfusion injury in hypertension.

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Cell culturing, ELISA, semi-quantitative RT-PCR, Western blotting.

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Calcium activated chloride channels (CaCCs) are critical in vascular smooth muscle function as they regulate proliferation/apoptosis of smooth muscle cells (SMCs) and vascular tone. Transmembrane protein 16A (TMEM16A) was demonstrated to encode CaCCs in basilar artery SMCs (BASMCs) and participate in basilar artery remodeling during hypertension. In addition, TMEM16A has recently been illustrated to contribute to pressure‑induced myogenic response in cerebral vasculature. However, whether TMEM16A is involved in cerebral vasoconstriction that is stimulated by other vasoconstrictors remains unclear. The aim of the present study was to establish whether TMEM16A is involved in the progression of angiotensin II (Ang II)‑induced basilar artery constriction and elucidate its potential role during hypertension. The study demonstrated that the specific inhibitor of TMEM16A, T16A‑inhA01 attenuated Ang II‑induced constriction in rat basilar arteries, and that this effect was weakened in parallel with the decline of TMEM16A expression in basilar arteries of 2‑kidney, 2‑clip hypertensive rats. Furthermore, it was found that 100 nM Ang II evoked a chloride current in cultured BASMCs with a basal 100‑nM intracellular Ca2+ ([Ca2+]i) level. In addition, the current could be abolished by TMEM16A small interfering RNA pretreatment and Ang II receptor type 1 (AT1) receptor blocker, losartan, while Ang II failed to cause a further increase to Ca2+‑dependent Cl‑ currents activated by 500 nM [Ca2+]i. In addition, in cultured BASMCs, Ang II induced phosphorylation of myosin phosphatase‑targeting subunit 1, and myosin light chains were significantly enhanced by TMEM16A overexpression, which were reversed by Rho‑associated protein kinase (ROCK) inhibitor, Y‑27632, while TMEM16A silencing demonstrated an opposing result. Furthermore, Ang II‑induced RhoA activation was enhanced by TMEM16A overexpression. In conclusion, the present study revealed that Ang II elicited a TMEM16A‑mediated current and TMEM16A participated in Ang II‑induced basilar constriction via the RhoA/ROCK signaling pathway.

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Diabetes mellitus (DM), which induces alterations in energy metabolism, is the leading cause of cardiovascular disease. We postulated that peroxisome proliferator activated receptor-gamma coactivator 1alpha (PGC-alpha), a transcriptional coactivator that is the primary regulator of oxidative metabolism and mitochondrial biogenesis, and cardiac function are depressive in DM and simvastatin and losartan therapy can improve the affects of DM on mRNA expression of PGC-1alpha and cardiac function. An experimental model of DM (induced by streptozocin 60 mg/kg) in adult male rats (n = 24) was used to investigate the mRNA expression of PGC-1alpha in the left ventricular myocardium. These rats were divided into group I (insulin therapy only, n = 8), group II (insulin plus simvastatin 20 mg/kg/day orally, n = 8), and group III (insulin plus losartan 20 mg/kg/day orally, n = 8). Diabetic rats and 8 healthy rats (group IV) were sacrificed at 3 weeks following DM induction. The mRNA expression of PGC-1alpha was measured using real-time polymerase chain reaction (RT-PCR). Additionally, transthoracic echocardiography was performed on days 0 and 21. The experimental results indicated that the mRNA expression of PGC-1alpha and the left ventricular ejection fraction (LVEF %) were significantly lower in groups I, II and III than in group IV (all P < 0.001). However, the mRNA expression of PGC-1alpha and the LVEF were significantly higher in group III than in groups I and II (both P < 0.01). Conversely, mRNA expression of PGC-1alpha and LVEF did not differ between groups I and II (P > 0.5). In conclusion, DM induces suppression of mRNA expression of PGC-1alpha and LV function in diabetic rats. Losartan and not simvastatin therapy improved the LV function and the expression of this mitochondrial-biogenesis regulator.

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Renin-angiotensin-aldosterone system (RAAS) blockade improves prognosis in renal patients, but usually requires diuretic co-treatment. RAAS blockade can decrease erythropoietin (EPO) and/or haemoglobin (Hb) levels. Diuretics decrease EPO in rodents, but their effect on EPO and Hb in humans is unknown.

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Tubulointerstitial fibrosis is considered to be common endpoint result of many forms of chronic renal diseases. Except for renal replacement, chronic renal fibrosis is presently incurable. This study demonstrates that the combination of hepatocyte growth factor (HGF) gene therapy with inhibition of the renin-angiotensin system produced synergistic beneficial effects leading to dramatic attenuation of renal tubulointerstitial fibrosis in obstructive nephropathy in mice. The combined treatment with human HGF gene and losartan, an angiotensin II (AngII) type I receptor blocker, preserved renal mass and gross morphology of the obstructed kidneys. Although HGF gene therapy alone inhibited the expression of alpha-smooth muscle actin (alpha SMA) by approximately 54% and 60% at day 7 and day 14 after surgery, respectively, its combination with losartan almost completely abolished alpha SMA induction in the obstructed kidneys. The combined therapy also synergistically inhibited the accumulation of interstitial matrix components, such as fibronectin and collagen I, and suppressed renal expression of transforming growth factor-beta1 (TGF-beta1) and its type I receptor. In vitro studies revealed that AngII by itself did not induce alpha SMA, but it drastically potentiated TGF-beta1-initiated alpha SMA expression in tubular epithelial cells. Furthermore, HGF abrogated de novo alpha SMA expression induced by TGF-beta1 plus AngII. These results suggest that many factors are implicated in the pathogenesis of renal interstitial fibrosis; therefore, a combined therapy aimed at simultaneously targeting multiple pathologic pathways may be necessary for halting the progression of chronic renal diseases. These findings may provide the basis for designing future therapeutic regimens for blocking progressive renal fibrosis in patients.

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We modified a rat model of exercise-induced renal injury by forcing 4-week-old male Sprague-Dawley (SD) rats (the MOD group) running on a treadmill for 8 weeks under conditions of high temperature, high humidity, bearing weight with some additional stimulations. Compared with the control (CON) group, the traditional running group (TRA), the losartan potassium intervention running group (LOS) and the traditional Chinese medicine "Yishen Huanji Decoction" intervention running group (CHI), the urinary, biochemistry indicators, the concentrations of angiotensin II (Ang II) were significantly higher in the MOD group than in the TRA group. After 3--4 weeks and 8-week training program, the 24-h urine protein and NAG levels in the LOS group and CHI group were lower than in the MOD group respectively. The BUN and SCr levels in the CHI group were lower than in the MOD group and higher than in the LOS group. AngII concentrations in the LOS group were higher than the MOD group. The modified rat renal injury model induced greater lesions than the traditional model. High temperatures, humidity and weight bearing were critical factors to induce Ang II activation, which can aggravate renal injury. Losartan potassium and the "Yishen Huanji Decoction" can protect against renal injury.

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Losartan and telmisartan, angiotensin AT1 receptor antagonists, are widely used antihypertensive drugs in patients. It is also known that arterial hypertension is often present in people with epilepsy, therefore, drug interactions between AT1 receptor antagonists and antiepileptic drugs can occur in clinical practice.

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Sodium hydrosulfide (NaHS, 56 µmol/kg/day) was administered intraperitoneally to the rats from the 7th day after 2K1C operation. Systolic blood pressure was significantly increased from the first week after the operation and was lowered after NaHS treatment for 4 weeks. H2S could also inhibit the ratio of left ventricle and septum weight to body weight, improve cross-sectional area, and ameliorate ventricular dysfunction. Additionally, the protein expression of AT1R and Ang II serum content were downregulated, whereas superoxide dismutase (SOD) protein was upregulated in 2K1C rats by NaHS treatment for 4 weeks. Furthermore, the reactive oxygen species level and AT1R protein were increased, whereas SOD protein was decreased in cardiomyocytes treated with Ang II compared with the control group. NaHS could reverse these changes. Losartan and N-acetylcysteine could also reverse Ang II-induced changes.

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cozaar drug class 2017-11-07

Angiotensin IV, [[des-Asp1,Arg2]ANG II or ANG-( buy cozaar 3-8)], has been shown to preferentially bind to a novel angiotensin binding site (AT4 receptor). The cellular location and function of this receptor in the rat kidney is unknown. Autoradiography localized AT4 receptors to the cell body and apical membrane of convoluted and straight proximal tubules in the cortex and outer stripe of the outer medulla. ANG IV (0.1 pM-1 microM) elicited a concentration-dependent decrease in transcellular Na+ transport (as measured by proximal tubule O2 consumption rates) in fresh suspensions of control or nystatin-stimulated (bypasses rate-limiting step of apical Na+ entry) rat proximal tubules. The inhibitory effect of 1 pM ANG IV was unaltered by either 1 microM losartan (AT1-receptor antagonist) or 1 microM PD-123319 (AT2-receptor antagonist) and yet was abolished by 1 microM divalinal-ANG IV (AT4-receptor antagonist) or ouabain pretreatment. These results demonstrate that the kidney AT4-receptor system is localized to the proximal tubule and suggests that one potential biological role of this system is in the regulation of Na+ transport by inhibiting a ouabain-sensitive component of Na(+)-K(+)-adenosinetriphosphatase activity in the rat.

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Aortic vascular smooth muscle cells (VSMC) from 12-week-old SHR and Wistar-Kyoto (WKY) rats were used for the present studies. The levels of inhibitory guanine nucleotide regulatory proteins (Gialpha-2 and Gialpha-3) and stimulatory proteins (Gsalpha) buy cozaar were determined by western blotting techniques. Adenylyl cyclase activity was determined by measuring [32P]cAMP formation from [alpha-32P]ATP.

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Our findings suggest that ECM depletion is an effective strategy to enhance buy cozaar the efficiency of viral vector-guided gene therapy.

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Effects were studied of a 6-week lozartan monotherapy, 50 mg daily, on the systemic hemodynamics, morphofunctional characteristics of the left ventricle (LV), lipid, carbohydrate, purin metabolisms, and some parameters characterizing renal function in patients with mild and moderately severe hypertensive disease (HD). A 24-h monitoring of arterial pressure (AP) was conducted in the above patients. Lozartan proved to be effective hypertensive medication in mild and moderately severe HD, capable of decreasing significantly total peripheral resistance with no reflex tachycardia developing. The drug has been shown to reduce nightly "pressure load" and AP in the buy cozaar small hours as well, and to improve the contractile and pumping function of the myocardium making for regression of LV hypertrophy, with no side effects noted.

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Screening costs per case for echocardiographic LVH are likely to be low, because of the high prevalence of the condition and the low unit cost of echocardiography. Treatment costs are likely to be comparable buy cozaar to those currently deemed acceptable in treating high-risk cardiovascular populations, e.g. the HOPE study population.

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Male ApoE(0) mice (50 buy cozaar -60 weeks) were randomly divided into 4 groups: saline, Ang II (1000 ng kg(-1) min(-1) for 4 weeks), Ang II plus antioxidants (0.1% vitamin E in food plus 0.1% vitamin C in drinking water), and Ang II plus losartan (30 mg kg(-1) day(-1)).

cozaar 60 mg 2016-12-23

We observed that autophagy (measured as LC3 staining, and Beclin-1 and p62 Western blotting) was an early response and apoptosis (measured as TUNEL staining, and Annexin V and Smac/Diablo Western blotting) became dominant as the duration of anoxia was prolonged. Autophagy also occurred quickly in response to low concentrations of Ang II. When exposed to high concentrations of Ang II, a buy cozaar significant number of cells developed apoptosis, while autophagy response decreased. Ang II-mediated apoptosis was blocked by Ang II type 1 receptor (AT1R) blocker losartan as well as by the AT2R blocker PD123319. Ang II-induced autophagy was blocked by losartan, but not by PD123319.

cozaar comp tablets 2015-10-27

The presence of buy cozaar ANGII receptors was assessed by binding studies. The effects of ANGII on intracellular calcium concentration ([Ca(2+)](i)), cell contraction, and cell proliferation were also assessed.

cozaar lethal dose 2017-03-25

Apolipoprotein E(-/-) mice were fed a high-fat, high-cholesterol (HFHC) diet for 12 weeks, with and without simvastatin (40 mg/kg) and/or losartan (20 mg buy cozaar /kg). The mice were divided into 5 groups and were fed as follows: regular chow (control diet, n=5), HFHC diet (n=6), HFHC diet with losartan (n=6), HFHC diet with simvastatin (n=6), and HFHC diet with both losartan and simvastatin (n=6).

cozaar 50 mg 2015-01-18

After two weeks, L-NAME induced high blood pressure, renal overexpression of AT1R, NAD(P)H oxidase sub-units gp91, p22 and p47, increased levels of oxidative stress, interleukin-6 (IL-6) and interleukin-17 (IL-17). Also, we found increased renal accumulation of lymphocytes and macrophages buy cozaar . Losartan treatment abolished the renal expression of gp91, p22, p47, oxidative stress and reduced NF-κB activation and IL-6 expression.

cozaar drugs 2017-04-18

Reduction in renal mass in rats results in progressive proteinuria, hypertension, focal-segmental glomerulosclerosis (FSG), atrophy of tubules (AT), and interstitial expansion. We reported that slow reduction of renal tissue in rats (slow ablation) ending in the removal of 1.5 kidneys is associated, over the next six months, with higher albumin excretion rates (AER) and accelerated development of FSG lesions compared to sudden equivalent buy cozaar renal mass reduction. It was hypothesised that slow reduction of nephron numbers allows for a process of conditioning of residual nephrons that increases their susceptibility to subsequent injury.

losartan cozaar reviews 2016-01-06

Although hypertension is the most common risk factor for thoracic aortic diseases, it is buy cozaar not understood how increased pressures on the ascending aorta lead to aortic aneurysms. We investigated the role of angiotensin II type 1 receptor activation in ascending aortic remodeling in response to increased biomechanical forces using a transverse aortic constriction (TAC) mouse model.

cozaar dosage 2016-03-27

We used immunostaining with characterized antibodies to study the localization of AT2 R in cultured human and rat dorsal root ganglion (DRG) neurons and a range of human tissues. The effects of AngII and AT2 R antagonist EMA401 on capsaicin responses in cultured human and rat (DRG) neurons buy cozaar were measured with calcium imaging, on neurite length and density with Gap43 immunostaining, and on cyclic adenosine monophosphate (cAMP) expression using immunofluorescence.

cozaar medication generic 2016-06-09

In the present study we assessed (1) the effects of 4 to 10 weeks of volume overload by an aortocaval shunt or minoxidil on LV and RV collagen and elastin and (2) the potential of the angiotensin- Avapro Brand Name converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan to prevent and regress volume overload-induced changes in cardiac collagen and elastin. Cardiac volume overload by aortocaval shunt or minoxidil treatment decreased LV collagen accumulation as compared with control rats. In contrast, RV collagen accumulation was potentiated during the initial weeks but not during chronic aortocaval shunt. Enalapril and losartan prevented the relative decreases in LV collagen content and concentration induced by a shunt. Losartan also reversed the decrease in LV collagen content by aortocaval shunt. Neither blocker significantly affected the enhanced RV collagen accumulation during the initial weeks of shunt, but both blockers further potentiated RV collagen accumulation during chronic volume overload. Aortocaval shunt for 4 weeks but not 10 weeks enhanced LV and RV elastin accumulation. This initial increase in LV and RV elastin content was blocked by both enalapril and losartan.

cozaar tabs 100mg 2016-10-25

We have previously shown, in a neonatal rat cell line, that angiotensin II (Ang II)-induced proliferation in vascular smooth muscle cells is extracellular matrix (ECM) dependent. We hypothesized that such an effect might be mediated via differences in Ang II-induced increases in the transcriptional factor early growth response-1 (Egr-1) gene and, consequently, in platelet-derived growth factor (PDGF). Cultured human newborn aortic smooth muscle cells were studied on 4 different surfaces: (1) plastic, (2) laminin, (3) collagen, and (4) fibronectin. Ang II-induced increases in DNA synthesis were significantly greater on collagen (2.0+/-0.3-fold) and fibronectin (1.9+/-0.3-fold) than on laminin (1.0+/-0.2-fold) or plastic (1.4+/-0.2-fold). As with DNA synthesis, at 48 and 72 hours, Ang II-induced increases in cell numbers occurred only in cells grown on collagen and fibronectin culture plates and were blocked by an antagonist to the angiotensin type 1 (losartan, 10 micromol/L) but not the angiotensin type 2 (PD 123319, 10 micromol/L) receptor. Anti-PDGF AA antibody (6 microg/mL) blocked the increase in DNA synthesis by 60% to 64% in cells on collagen or fibronectin cultures but not on plastic cultures. When PDGF-AA (10 ng/mL) and Ang II were added together, DNA synthesis increased 2-fold and did not differ on the various ECM proteins. Increases in PDGF A-chain mRNA were observed only in cells grown Kemadrin Dose on collagen (3.21+/-0.65-fold) and fibronectin (2.86+/-0.49-fold) plates 2 to 8 hours after the addition of Ang II and were blocked by losartan but not PD 123319. Expression of Egr-1, an early growth response gene, increased at 15 minutes, peaked at 30 minutes, and returned to normal after 2 hours with Ang II treatment. Ang II-induced increases in Egr-1 mRNA were greater on collagen (4. 82+/-0.66-fold at maximum) and fibronectin (4.01+/-0.56-fold) than on laminin (2.74+/-0.45-fold) or plastic (2.53+/-0.40-fold) and were blocked by losartan but not PD 123319. Thus, in human vascular smooth muscle cells in culture, Ang II-induced proliferation is mediated via the angiotensin type 1 receptor, dependent on ECM proteins, and regulated by differential gene expression of Egr-1 and PDGF-1.

cozaar generic name 2016-02-05

It is suggested that combined therapy of ACEi and ARB with relatively high or maximal doses Trileptal With Alcohol of each drug has no additive or synergistic benefits on the progression of ADR-induced glomerulopathy. Effects of RAS blockade may in part be related to differential regulation of type 1 and type 2 angiotensin II receptors.

cozaar 25 mg 2017-04-21

We enrolled 15 patients with severe heart failure due to nonischemic cardiomyopathy and with no histologic evidence of active myocarditis. All had markedly reduced cardiac output and were receiving inotropes. The patients underwent implantation of left ventricular assist devices and were Imodium Capsules treated with lisinopril, carvedilol, spironolactone, and losartan to enhance reverse remodeling. Once regression of left ventricular enlargement had been achieved, the beta2-adrenergic-receptor agonist clenbuterol was administered to prevent myocardial atrophy.

losartan cozaar generic 2016-10-13

TLR4, NF-kappaB, IL-6,and TNF-alpha were highly expressed in AngII induced NRK-52E(P<0.01). In NRK-52E that was stably transfected TLR4-special RNAi plamids, TLR4 protein and mRNA expression were obviously inhibited(P<0.05). After Trileptal Starting Dose stimulation by AngII, the TLR4, IL-6, TNF-alpha levels in the stabe transfection group were increased compared with the normal group(P<0.05). Fos or/and Los down-regulated TLR4, IL-6, and TNF-alpha expressions(P<0.05), but no cooperation was observed.

cozaar dose 2015-07-31

Treatment of HIV infection with potent combination antiretroviral therapy has resulted in major improvement in overall survival, immune function and the incidence of opportunistic infections. However, HIV infection and treatment has been associated with the development of metabolic complications, including hyperlipidaemia, diabetes mellitus, hypertension, lipodystrophy and osteopenia. Safe pharmacological treatment of these complications requires an understanding of the drug-drug interactions between antiretroviral drugs and the drugs used in the treatment of metabolic complications. Since formal studies of most of these interactions have not been performed, predictions must be based on our understanding of the metabolism of these agents. All HIV protease inhibitors are metabolised by and inhibit cytochrome P450 (CYP) 3A4. Ritonavir is the most potent inhibitor of CYP3A4. Ritonavir and nelfinavir also induce a host of CYP isoforms as well as some conjugating enzymes. The non-nucleoside reverse transcriptase inhibitor delavirdine potently inhibits CYP3A4, whereas nevirapine and efavirenz are inducers of CYP3A4. Drug interaction studies have been performed with HIV protease inhibitors and HMG-CoA reductase inhibitors. Coadministration of ritonavir plus saquinavir to HIV-seronegative volunteers resulted in increased exposure to simvastatin acid by 3059%. Atorvastatin exposure increased by 347%, but exposure to active atorvastatin increased by only 79%. Conversely, pravastatin exposure decreased by 50%. Similar results have been obtained with combinations of simvastatin and atorvastatin with other HIV protease inhibitors. Thus, the lactone prodrugs simvastatin and lovastatin should not be used with HIV protease inhibitors. Atorvastatin may be used with caution. Although there are no formal studies available, calcium channel antagonists and repaglinide may have significant interactions and toxicity when used with HIV protease inhibitors because of their metabolism by CYP3A4. Sulfonylurea drugs utilise mainly CYP2C9 for metabolism, and this isoenzyme may be induced by ritonavir and nelfinavir with a resulting decrease in efficacy of the sulfonylurea. Losartan may have increased effect when coadministered with ritonavir and nelfinavir because of the induction of CYP2C9 and the expected increase in formation of the active metabolite, E-3174. Overall, well-designed drug-drug interaction studies Cymbalta Overdose Symptoms at steady state are needed to determine whether antiretroviral drugs may be safely coadministered with many of the drugs used in the treatment of the metabolic complications of HIV infection.

cozaar generic price 2016-05-06

Podocyte stress precedes proteinuria in hypercholesterolemic rats. Molsidomine, a nitric oxide (NO) donor, prevented podocyte stress and proteinuria in long-term hypercholesterolemia, suggesting that podocyte stress was due to NO deficiency. Podocytes express the angiotensin II type 1 receptor, which influences their function. Because NO counteracts angiotensin II, it was hypothesized that in a setting of impaired renal NO availability, angiotensin II receptor inhibition could prevent podocyte stress. For determining the effect of NO deficiency on podocyte stress, one group of Tegretol Overdose female rats were fed 2% cholesterol and another group the arginine analogue N-omega-nitro-L-arginine (L-NNA; 40 mg/kg food) for 2 wk. Another group of rats that were fed 2% cholesterol also received the NO donor molsidomine (120 mg/L water) for 2 wk before and during cholesterol feeding. For determining the influence of angiotensin II in the setting of decreased renal NO availability, rats that were treated with cholesterol or L-NNA received the angiotensin II type 1 antagonist losartan (200 mg/L water) for 2 wk before and during cholesterol or L-NNA administration. Desmin staining and electron microscopy were used to monitor podocyte activation. Glomerular caveolin was quantified by immunohistochemistry. Renal cortical NO synthesis, NO synthase isoforms, and caveolin-1 protein mass were also measured. Both short-term cholesterol and L-NNA induced podocyte stress as evidenced by enhanced desmin staining and electron-dense fused foot processes. Podocyte stress was prevented by molsidomine in short-term hypercholesterolemia. Furthermore, losartan prevented podocyte stress in rats that were treated with cholesterol or with L-NNA. Finally, hypercholesterolemia decreased renal cortical NO synthase activity and increased caveolin-1 protein mass and glomerular caveolin staining, and these changes were also prevented by losartan. It is suggested that podocyte stress in these models of early injury results from angiotensin II, unopposed by the action of endogenous NO. This underscores the strategic role of angiotensin II blockers in early kidney disease.

cozaar cost 2015-06-05

Combined high-dose angiotensin II receptor blocker to high-dose angiotensin-converting enzyme inhibitor therapy is safe and effective in reducing Detrol Er Dosage proteinuria in childhood SRNS. However a large-scale study should be conducted to validate this result.

cozaar double dose 2015-06-05

In Voltaren Brand Name light of our findings, losartan may be a useful option in CED management.

cozaar y alcohol 2016-01-24

Our findings suggest Protonix Generic Price that paricalcitol treatment counteracts increased contrast induced nephropathy caused by losartan. These findings warrant further clinical studies to investigate the benefit of paricalcitol in CIN prophylaxis.

cozaar medication picture 2016-12-17

We recently reported a series of 1-acyl-N-(biphenyl-4-ylmethyl)pyrrolidine-2-carboxamides as AT(1) receptor ligands. The most potent compound of the series, 1-pentanoyl-N-{[2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl}-pyrrolidine-2-carboxamide, showed an interesting affinity for the receptor. To investigate the influence of structure variations on affinity, the synthesis of additional compounds belonging to this series has been performed. Biological tests run on the newly synthesized Arava Generic Name compounds on CHO-hAT(1) cells stably expressing the human AT(1) receptor confirm our previous hypothesis, i.e. that, within this series, the length of the acyl chain, the substitution of the amidic group and the nature of the acidic one are crucial for the receptor interaction, being a valeric chain, a secondary amidic function and the tetrazole moiety, respectively, the optimal ones.