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jelfa omnadren 250 Steroids 

jelfa omnadren 250

PHARMACOLOGICAL PROPERTIES OF MECHANISM OF ACTION components Jelfa omnadren 250 drug additive have an antihypertensive effect, reducing blood pressure (BP) to a greater degree than each of the components individually. Due to diuretic hydrochlorothiazide effect increases plasma renin activity (PRA), stimulates the secretion of aldosterone, angiotensin II increases and decreases the level of potassium in serum. Losartan blocks all the physiological effects of angiotensin II and aldosterone effects due to the suppression reduces the loss of potassium caused by diuretic. Losartan has a mild and transient uricosuric effect. Hydrochlorothiazide causes a slight increase in the level of uric acid in the blood; the combination of losartan and hydrochlorothiazide reduces the severity of hyperuricemia caused by diuretic.


Jelfa omnadren 250 is a combination of losartan (COZAAR) and hydrochlorothiazide. In patients with hypertension and left ventricular hypertrophy, losartan, often in combination with hydrochlorothiazide reduces the risk of cardiovascular morbidity and mortality, which has been proven by evaluating the combined incidence of cardiovascular death, stroke and myocardial infarction in this group of patients (study RACE).

while taking losartan the removal of the negative feedback is to suppress angiotensin II renin secretion leads to increased blood plasma renin activity (PRA). ATM growth is accompanied by an increase in angiotensin II in the blood plasma. With long-term (6-week) treatment of hypertensive patients with losartan 100 mg / day, when maximum drug concentration in plasma was observed a 2-3 fold increase in the level of angiotensin II in the blood plasma. Some patients showed even greater, especially if short duration of treatment (2 weeks). However, antihypertensive activity and reduced aldosterone plasma concentrations were shown at 2 and 6 weeks of treatment, indicating that effective blockade of angiotensin II receptors. ATM and angiotensin II levels declined to baseline values observed prior to administration of the drug after 3 days after withdrawal of losartan. Jelfa omnadren 250a impact on the ATM and angiotensin II level was comparable to that when receiving 50 mg of losartan.
As specific antagonist is losartan AT 1 receptor of angiotensin II, it does not inhibit ACE (kininase II) – an enzyme that inactivates bradykinin. A study which compared the effects of 20 mg and 100 mg of losartan potassium with an ACE inhibitor effects on the response to angiotensin I, angiotensin II and bradykinin indicated that losartan blocks the effects of angiotensin I and angiotensin II, without influencing the effects of bradykinin. These results are consistent with the specificity of action of losartan. In contrast, ACE inhibitor, blocked the response to angiotensin I and increased severity of the response to bradykinin, without affecting the intensity of the response to angiotensin II, which demonstrates the pharmacodynamic difference between losartan and ACE inhibitors.
The concentrations of losartan and its active metabolite in plasma, and the antihypertensive effect of losartan increase with increasing dose. Since losartan and its active metabolite are antagonists of angiotensin II receptors, both of them contribute to the antihypertensive effect.
In a clinical study with a single dose of 100 mg of losartan potassium, which is included in healthy volunteers (male), the introduction of the drug in a diet high and malosolevoy It had no effect on glomerular filtration rate (GFR), effective renal plasma flow and filtration fraction. Losartan has a natriuretic effect which was more pronounced at malosolevoy diet and, apparently was not associated with suppression of early sodium reabsorption in the proximal renal tubules. Losartan also causes a transient increase in the excretion of uric acid by the kidneys.
In patients with hypertension, proteinuria ( > 2 g / 24 hours), non-diabetic and taking 8 weeks losartan 50 mg, with a gradual increase to 100 mg, there was a significant reduction proteinuria by 42%.Fractional excretion of albumin and IgG also significantly decreased. In these patients, losartan stabilized GFR and decreased filtration fraction.
In postmenopausal women with hypertension treated with losartan potassium 50 mg / day for 4 weeks, showed no effect of therapy on renal and systemic levels of prostaglandins.
Losartan has no effect on autonomic reflexes and has a prolonged effect on the level of noradrenaline in the blood plasma.
in patients with hypertension losartan at doses up to 150 mg / day did not cause clinically significant changes in fasting triglyceride levels, total cholesterol and high density lipoprotein (HDL). At the same doses losartan did not affect the blood glucose level on an empty stomach.
In general, losartan caused a decrease in serum uric acid levels (generally less than 0.4 mg / dl), persisted during prolonged therapy. In controlled clinical trials, in which included patients with hypertension cases of discontinuation due to an increase in creatinine levels, or potassium blood serum have been reported.
The 12-week, parallel study, which included patients with left ventricular failure (II-IV functional class classification NYHA) and most of them were diuretics and / or digitalis, compared the effects of losartan in doses of 2.5, 10, 25 and 50 mg daily with placebo. At doses of 25 mg and 50 mg per day of the drug has positive hemodynamic and neurohormonal effects that were observed throughout the study.Hemodynamic effects included an increase in cardiac index and a decrease in wedge pressure in the pulmonary capillaries, as well as a decrease in systemic vascular resistance, mean systemic arterial pressure and heart rate (HR). The incidence of hypotension in these patients depended on the dose of the drug. Neurohormonal effects included a decrease in the level of aldosterone and norepinephrine in the blood.


Absorption Losartan When administered losartan is well absorbed and metabolized at a “first pass” through the liver, resulting in formation of the active carboxylated metabolite and inactive metabolites.Losartan Systemic bioavailability in tablet form is approximately 33%. Mean maximum concentrations of losartan and its active metabolite are achieved over 1 hour, 3-4 hours, respectively. When losartan mealtime clinically significant effect on the profile of losartan plasma concentrations were identified.

Distribution Losartan Losartan and its active metabolite is bound to plasma proteins (mainly albumin) is greater than 99%. The volume of distribution of losartan is 34 liters. Studies in rats have shown that losartan does not penetrate the blood-brain barrier. Hydrochlorothiazide Hydrochlorothiazide crosses the placental (but not the blood-brain) barrier and is excreted in breast milk. Metabolism Losartan About 14% of the dose of losartan administered intravenously or by mouth, is converted into its active metabolite. After oral and intravenous administration of losartan, labeled with  14 C radioactivity circulating plasma primarily due to the presence therein of losartan and its active metabolite. In addition to the active metabolite form of biologically inactive, including two major metabolite resulting from hydroxylation of the butyl side chain, and secondary one – N-2-tetrazol-glucuronide. how much to inject for weight loss

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