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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:
Acetensa, Angibloc, Angilock, Angioten, Angizaar, Anreb, Anreb plus, Ara ii, Aralo x, Arapres, Aratan, Araten, Asart, Biortan, Cardizaar, Cardon, Cardoplus, Cardzaar, Cartan, Co-losar, Combizard, Cormac, Corodin, Corus, Cosart, Covance, Cozaarex, Cozzar, Czartan, Eklips, Enromic, Etan, Faxiven, Fensartan, Fortzaar, Forzaar, Giovax, Gitox, Hilos, Hizaar, Hypozar, Insaar, Klosartan, Lacine, Lakea, Lara, Larb, Larb plus, Lavestra, Lepitrin, Lifezar, Loben, Loctenk, Logika, Lohyp, Loortan, Lopernal, Loplac, Lopo, Lopress, Lorista, Los-arb, Losa, Losacar, Losachlor, Losacor, Losacor plus, Losadel, Losadrac, Losagen, Losalet, Losamet, Losan, Losan d, Losap, Losapot, Losapres, Losaprex, Losar, Losar-q, Losarb, Losardil, Losardil plus, Losargamma, Losarquilab, Losart, Losart plus, Losartanum, Losartas, Losartax, Losartec, Losartic, Losartil, Losatan, Losatrix, Losavik, Losazid, Losazide, Losium, Lospre, Lostad, Lostan, Lostankal, Lotan, Lotar, Lotim, Loxibin, Lozap, Lozar, Lozatan, Lozitan, Lyosan, Maxartan, Medzar, Mozartan, Myotan, Nefrotal, Neo lotan, Niten, Normatens, Nu-lotan, Ocsaar, Osartan, Osartan hz, Osartil, Osartil plus, Ostan, Ozarium, Portiron, Prelow, Prosan, Psycholanz, Ranlozar, Rasertan, Rasoltan, Repace, Resilo, Rosatan, Sanipresin, Sarilen, Sarlo, Sartaxal, Sartens, Sarvas, Sarvastan, Sarve, Satoren, Sedeten, Simperten, Sortal, Sortiva, Stadazar, Tacardia, Tacicul, Tanlozid, Tarnasol, Temisartan, Tensaar, Tensartan, Tensiohess, Tiasar, Tozaar, Vilbinitan, Xartan, Zaart, Zartan

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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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Brain renin-angiotensin system (RAS) could regulate oxidative stress in the paraventricular nucleus (PVN) in the development of hypertension. This study was designed to explore the precise mechanisms of RAS acting on reactive oxygen species (ROS) in salt-induced hypertension. Male Wistar rats were administered with a high-salt diet (HS, 8.0% NaCl) for 8 weeks to induced hypertension. Those rats were received PVN infusion of AT1R antagonist losartan (LOS, 10 μg/h) or microinjection of small interfering RNAs for protein kinase C γ (PKCγ siRNA) once a day for 2 weeks. High salt intake resulted in higher levels of AT1R, PKCγ, Rac1 activity, superoxide and malondialdehyde (MDA) activity, but lower levels of copper/zinc superoxide dismutase (Cu/Zn-SOD), superoxide dismutase (SOD) and glutathione (GSH) in PVN than control animals. PVN infusion of LOS not only attenuated the PVN levels of AT1R, PKCγ, Rac1 activity, superoxide and decreased the arterial pressure, but also increased the PVN antioxidant capacity in hypertension. PVN microinjection of PKCγ siRNA had the same effect on LOS above responses to hypertension but no effect on PVN level of AT1R. These results, for the first time, identified that the precise signaling pathway of RAS regulating ROS in PVN is via AT1R/PKCγ/Rac1 in salt-induced hypertension.

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Significant innovations have defined the approach to the proximal thoracic aorta. Aortic proteolysis predisposes to dissection and aneurysm. Losartan may prevent aortic root dilation in Marfan syndrome. The Loeys-Dietz syndrome mandates early aortic intervention. Because genetic aortopathies have a multicenter registry, further aortic molecular advances are likely. Acute intramural hematoma (IMH) may be due to aortic dissection with unrecognized microintimal tears. Type-A IMH is often a surgical emergency, whereas type-B IMH often requires medical management. Because preoperative ischemia predicts mortality in type-A dissection, it is logical to classify this disease by ischemic presentation. Because advanced age worsens the outcome in type-A dissection, transcatheter interventions should be urgently developed for this high-risk subgroup. Aortic arch repairs shorter than 45 minutes in duration are safely performed under deep hypothermic circulatory arrest with/without perfusion adjuncts. Bilateral antegrade cerebral perfusion (ACP) offers the best neuroprotection for complex repairs longer than 45 minutes. Axillary artery cannulation improves outcomes in proximal thoracic aortic procedures. Contralateral hemispheric ischemia is possible with unilateral ACP because cross-cerebral perfusion may be inadequate. Arch repair with ACP and moderate HCA is safe and effective and represents a research opportunity for pharmacologic ischemic preconditioning. Antegrade thoracic aortic stenting for DeBakey 1 dissection thromboses the distal false lumen to improve long-term aortic outcomes. Endovascular arch repair is feasible and may soon be done off-pump. These described innovations have collectively ushered in a paradigm shift in diseases affecting the ascending aorta and aortic arch.

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TLR4 may lead to inflammatory reaction in hypertensive renal injury. Fos or/and Los can decrease the expressions of TLR4 and correlate inflammatory factors, which may be part of the renal protective mechanism.

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We communicated the central effect of angiotensin III (ANG III), a potent signal for extracellular dehydration, on single neurons in the caudal hypoglossal nucleus of Sprague-Dawley rats anesthetized with pentobarbital sodium. A significant number (121 of 168) of caudal hypoglossal neurons responded to intracerebroventricular application of ANG III (80 or 160 pmol), with either an increase (n = 83) or decrease (n = 38) in their spontaneous discharge. These effects of ANG III were significantly reversed by intracerebroventricular application of the nonpeptide angiotensin AT1 receptor antagonist losartan (40 nmol), but not by the AT2 antagonist, PD-123319. The hypoglossal neuronal responses to repeated administration of ANG III (80 pmol), delivered at an interval < or = 18 min, exhibited acute tachyphylaxis. Intracerebroventricular administration of the cholinergic dipsogen, carbachol (50 ng), or the osmotic stimulant, hypertonic saline (0.5 M), also elicited responses in ANG III-responsive hypoglossal neurons. These results suggest that neurons in the caudal hypoglossal nucleus may serve as the final common pathway for extracellular and, possibly, intracellular thirst in the rat. Furthermore, it is likely that the action of ANG III is mediated by the AT1 subtype of angiotensin receptors.

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To assess the effects of pharmacological interruption of the renin-angiotensin system on the fibrinolysis, tissue plasminogen activator antigen (t-PA), plasminogen activator inhibitor-1 antigens (PAI-1) and neurohormones, such as plasma renin activity, norepinephrine, angiotensin II (AII) and IV (AIV) concentrations, were measured in 60 hypertensives. Among them, 48 patients were divided into two groups (25 with 10-20 mg quinapril and 23 with 50-100 mg losartan) who received the drug for 6 months. AII had a weak positive correlation with free PAI-I (n = 60, r = 0.26, p < 0.05) whereas AIV had a strong positive correlation with free PAI-I (n = 60, r = 0.57, p < 0.0001). In both treatment groups, blood pressures were significantly reduced to similar levels after drug treatment. While plasma renin activity increased significantly in both groups after drug treatment, only the losartan group showed significant increases in AII and AIV concentrations. In the quinapril group, there was a significant change in t-PA (p < 0.001) without changes in PAI-1. In the losartan group, free PAI-I and total PAI-I (p < 0.05 for free PAI-I and p < 0.04 for total PAI-I) were significantly increased without a change in t-PA. Thus, quinapril enhanced fibrinolysis but losartan attenuated it. These unique effects of each drug on the fibrinolytic system appear to be associated with changes in AII and AIV concentrations.

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Reverse transcriptase-polymerase chain reaction was performed to determine the expression of angiotensinogen, renin, angiotensin-converting enzyme and angiotensin receptor subtype 1 mRNA. The presence of AngII in ureteral tissue was determined by immunohistochemistry. Human and pig ureteral smooth muscle strips were suspended in tissue baths to determine the effect of the AngII receptor antagonist losartan on the frequency and amplitude of spontaneous ureteral contractions. Electrical field stimulation was performed before and after exposure to losartan.

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These results support the importance of cross-talk among different cell types in the regulation of vascular or renal function. ET-1, and particularly ECE-1, might constitute a target in this regulation. In addition, locally synthesized AII could be one of the mediators involved in the down-regulation of ECE-1.

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The left ventricular midwall shortening-circumferential end-systolic stress relationship in 45 normotensive Wistar rats was used to calculate the ratio of observed to predicted left ventricular midwall fractional shortening. At the endpoint, afterload-independent midwall shortening was higher in Dahl S rats on losartan or tap water, and in Dahl R rats on losartan than in weight-matched normotensive Wistar rats (all P<0.05). Afterload-independent midwall shortening was related to the left ventricular chamber dimension in a learning series of 109 rats (64 Goldblatt and 45 normotensive rats on a normal sodium diet; r = 0.73) and was adjusted in Dahl rats to a constant left ventricular internal diameter (6.9 mm) by the learning regression equation. The adjusted afterload-independent midwall shortening was still higher in Dahl S rats on losartan than in controls (P<0.02). Left ventricular internal diameter-adjusted afterload-independent midwall shortening was inversely related to the left ventricular mass in both Dahl S and Dahl R groups (r = -0.40 and -0.72, both P<0.04).

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Appreciation of the role of aldosterone in cardiovascular and renal disease has increased in the last 50 years. The use of spironolactone was limited by adverse sexual effects, including gynaecomastia. Eplerenone is a newer aldosterone antagonist that is much more selective, with minimal affinity for progesterone and androgenic receptors; therefore, there are very few reports of adverse sexual effects. A review of published trials shows that eplerenone reduces blood pressure (BP) in a dose-dependent manner, from 50 to 200 mg/day, and to a similar degree as enalapril. It has an additive effect when given to patients inadequately controlled on an angiotensin-converting enzyme inhibitor or an angiotensin-receptor blocker. Eplerenone performs better than losartan in African-American patients and lowers BP regardless of initial plasma renin activity. The risk of hyperkalaemia is low, similar to that of enalapril, and < 1% of patients have had to be withdrawn from studies because of elevated serum potassium levels. Eplerenone is an effective, well-tolerated antihypertensive agent that may be used alone or in conjunction with other agents; apart from the risk of hyperkalaemia, adverse effects are similar to placebo.

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Despite progress in the detection and treatment of hypertension the percentage of patients with controlled hypertension has failed to increase. The problem of poor blood pressure control is even more serious in elderly hypertensives than in the rest of the population. The antihypertensive drugs of the AIIRA (non-peptide angiotension II receptor antagonist) class are drugs whose use and experience are increasing and whose properties make them particularly useful in the elderly. We tried to assess the efficacy of treatment with losartan, the first AIIRA drug in a cohort of elderly patients with essential hypertension and to assess the percentage of patients achieving optimum BP control and to evaluate its safety, tolerability and metabolic effects. The intervention proved to be highly effective, achieving the anticipated blood pressure levels in the elderly in 77% of subjects after a 16-week follow-up, with very good tolerability. Renal function remained unchanged, as did the subjects' lipid profile.

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An ARB combined with an ACE inhibitor may benefit heart failure patients who are receiving all other recommended therapies. Further trials are needed to evaluate long-term safety effectiveness, quality of life, and survival before the combination can be recommended for routine use.

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Radiation-induced optic nerve damage was reduced by ramipril, a prodrug angiotensin-converting enzyme inhibitor (ACEI). This study was to determine the optimum dose and administration time of ramipril for mitigating radiation-induced optic neuropathy.

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Nuclear factor-kappa B (NF-kappaB) is a potent inducer of pro-inflammatory cytokines (PIC) and oxidative stress in cardiovascular disease. In this study, we Generic Avodart Uk determined whether upregulation of NF-kappaB in the hypothalamic paraventricular nucleus (PVN) contributed to neurohumoral excitation either directly, or via interaction with the renin-angiotensin system (RAS), in heart failure (HF).

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The process of cardiac hypertrophy is considered to involve two components: that of cardiac myocyte (CM) enlargement and cardiac fibroblast (CF) proliferation. The interleukin-6 (IL-6) family cytokines have been implicated in a variety of cellular and molecular interactions between myocytes and non-myocytes Nexium Generic Otc (NCMs), which in turn have important roles in the development of cardiac hypertrophy. In the study of these interactions, we previously detected very high levels of IL-6 in supernatants of a "dedifferentiated model" of adult ventricular CMs cultured with CFs. In the present study, we have used this in vitro coculture system to examine how IL-6 is involved in the interactions between CMs and CFs during CM hypertrophy and CF proliferation. IL-6 and its signal transducer, 130-kDa glycoprotein (gp130), were detected by immunostaining cultured CMs and CFs with anti-IL-6 or anti-gp130 antibodies. Addition of anti-IL-6 or anti-gp130 antagonist antibodies into CM/CF cocultures induced a significant decrease in expression of atrial natriuretic peptide (ANP) and beta-myosin heavy chain (beta-MHC) in CMs. The presence of IL-6 antagonist also resulted in a decrease in the surface area of 12-day-old CMs cultured with CFs or in the presence of fibroblast conditioned medium (FCM), and decreased fibroblast proliferation in CM/CF cocultures, particularly in the presence of a gp130 antagonist. The results also show that angiotensin II (AngII) is mainly secreted by CFs and induces IL-6 secretion in CMs cultured with CFs or with FCM. In addition, the effects of IL-6 on cardiomyocyte hypertrophy and fibroblast proliferation were inhibited by addition of the AT-1 receptor antagonist, losartan. These results suggest that IL-6 contributes significantly to CM hypertrophy by an autocrine pathway and to fibroblast proliferation by a paracrine pathway and that these effects could be mediated by AngII.

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Our data reinforce the superiority of a standardized upright ARR as a screening test in the diagnosis of primary aldosteronism, identifying 40 as an ideal cut-off value. Saline infusion represents a useful test to confirm such a diagnosis, Duricef Generic with a serum aldosterone level of 7 ng/dl as a satisfactory cut-off value. Some more information is obtained when the aldosterone/cortisol ratio is considered.

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Signaling through both angiotensin AT1 receptors (AT1R) and dopamine D1 receptors (D1R) modulates renal sodium excretion and arterial BP. AT1R and D1R form heterodimers, but whether treatment with AT1R antagonists functionally modifies D1R via allosterism is unknown. In this study, the AT1R antagonist losartan strengthened the interaction between AT1R and D1R and increased expression of D1R on the plasma membrane in vitro. In rat proximal tubule cells that express endogenous AT1R and D1R, losartan increased cAMP generation. Losartan increased cAMP in HEK 293a cells transfected with both AT1R and D1R, but it did not increase Keflex Cost cAMP in cells transfected with either receptor alone, suggesting that losartan induces D1R activation. Furthermore, losartan did not increase cAMP in HEK 293a cells expressing AT1R and mutant S397/S398A D1R, which disrupts the physical interaction between AT1R and D1R. In vivo, administration of a D1R antagonist significantly attenuated the antihypertensive effect of losartan in rats with renal hypertension. Taken together, these data imply that losartan might exert its antihypertensive effect both by inhibiting AT1R signaling and by enhancing D1R signaling.

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VSMC from SHR exhibited enhanced expression of Gialpha-2 and Gialpha-3 proteins as compared with age-matched WKY rats; however, the levels of Gsalpha proteins were not different between the two groups. The levels of superoxide anion (O2-) were also increased in SHR as compared with WKY rats, and losartan, an AT1 receptor antagonist, restored the enhanced levels to control WKY rat levels. Treatment of VSMC with antioxidants such as N-acetyl-L-cysteine (NAC) or diphenyleneiodonium (DPI) for 24 h decreased the enhanced expression of Gialpha-2 and Gialpha-3 proteins in a concentration-dependent manner in VSMC from SHR. In addition, the inhibition of forskolin-stimulated enzyme activity by low concentrations of GTPgammaS (receptor-independent Gi functions) and C-ANP4-23-mediated inhibition of adenylyl cyclase (receptor-dependent Gi functions) that were significantly enhanced in SHR were restored to WKY rat levels by NAC and DPI treatments. Similarly, diminished stimulation of adenylyl cyclase by GTPgammaS, isoproterenol and sodium fluoride in SHR was also restored towards control WKY rat levels by NAC and DPI treatments. Furthermore, PD98059, a selective inhibitor of mitogen-activated protein kinase Neurontin Online , was able to restore the enhanced expression of Gialpha proteins in VSMC from SHR towards WKY rat levels. In addition, the enhanced activity of extracellular signal-regulated kinase 1/2 in SHR as compared with WKY rats, as demonstrated by enhanced phosphorylation of extracellular signal-regulated kinase 1/2, was also restored to WKY rat levels by NAC or DPI.

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In IR group: UCP2 protein but not mRNA level was increased in the ischemic area of the left ventricle (LV) (172% ± 26.7, p < 0.001 vs. LV of control). Following acute myocardial IR, UCP2 protein levels was increased in the ischemic area of the LV but not in RV, suggesting the local effect of ischemia on UCP2 expression. IR-induced overexpression of UCP2 was Epivir Generic suppressed by ramiprilat and losartan.

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The effect of angiotensin II (Ang II) on Ca(2+) signalling in human primary cultured breast epithelial cells was investigated by using fura-2 as the Ca(2+) probe. Ang II (0.1-1000 nM) induced an intracellular free calcium ([Ca(2+)](i)) transient peak which was unchanged by external Ca(2+ )removal. In Ca(2+)-free medium pretreatment with thapsigargin abolished Ang II-induced Ca(2+ )release. Suppression of 1,4,5-inositol trisphosphate formation by U73122, a phospholipase C inhibitor, blocked the Ang II-induced Ca(2+) response. Losartan (DuP753), an inhibitor of Ang II type I receptor (AT1), decreased the [Ca(2+)](i) increase evoked by Ang II, while CGP4221A, an inhibitor of Ang II type II receptor (AT2) did not. AT1 desensitisation was demonstrated with respect to the Ca(2+) response after subsequent exposure of cells to Ang II and also after pretreatment for 25 min with 1000 nM phorbol 12-myristate 13-acetate. Staurosporine, an inhibitor of protein kinases C (PKC), inhibited the AT1 desensitisation. Epithelial breast cells expressed PKC-alpha, -beta1, -delta and -zeta isozymes, and Ang II provoked translocation from the cytosol to the membranes of PKC-alpha, -beta1, and -delta (but not -zeta). Ang II was also able to stimulate cell proliferation in a dose-dependent manner; this effect was blocked by Gö 6976, a specific inhibitor of PKC-alpha and -beta1, the Ca(2+)-dependent isozymes. The main conclusion of this study is that the the Ang II signalling mechanism in breast epithelial cells is based on the elevation of [Ca(2+)](i )released from intracellular stores through AT1 activation. In addition, Ang II stimulates cell proliferation by the activation Feldene Gel Purchase of PKC isozymes.

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We randomized 24 adult cardiac troponin T (cTnT-Q(92)) mice, which exhibit myocyte disarray and interstitial fibrosis, to treatment with losartan or placebo and included 12 nontransgenic mice as controls. The mean dose of losartan and the mean duration of therapy were 14.2+/-5.3 mg. kg(-1). d(-1) and 42+/-9.6 days, respectively. Mean age, number of males and females, and heart/body weight ratio were similar in the groups. Collagen volume fraction and extent of myocyte disarray were increased in the cTnT-Q(92) mice (placebo group) compared with nontransgenic mice (9.9+/-6.8% versus 4.5+/-2 Crestor Generic Cost .2%, P=0.01, and 27.6+/-10.6% versus 3.9+/-2.3%, P<0.001, respectively). Treatment with losartan reduced collagen volume fraction by 49% to 4.9+/-2.9%. The expression of collagen 1alpha (I) and transforming growth factor-beta1, a mediator of angiotensin II profibrotic effect, were also reduced by 50%. Losartan had no effect on myocyte disarray.

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Postoperative atrial fibrillation is a well recognized complication after lung cancer surgery, with an incidence as high as 30%. Perioperative increase of NT-proBNP has been demonstrated to be a strong independent predictor of postoperative atrial fibrillation in this setting.