anadrol dosage

Anadrol dosage antihypertensive drug, a specific angiotensin II receptor antagonist. Selectively acts on the AT1 receptor subtype, which is responsible for the known effects of angiotensin II.
The active hormone of the renin-angiotensin-aldosterone system is angirtenzin II, which is formed from angiotensin I, with the participation angiotenzinprevravdayuschego enzyme.

Angiotensin II binds to specific receptors on cell membranes in various tissues. It has a wide range of physiological effects, including, in particular, as a direct or indirect involvement in the regulation of blood pressure (BP). As a potent vasoconstrictor, angiotensin II causes a direct pressor response. In addition, it contributes to the delay of sodium ions in the body, and stimulates the secretion of aldosterone.
The affinity of valsartan receptor subtype AT1 much (about 20 000 times) higher than for the receptors subtype.
Valsartan does not inhibit ACE, also known as kininase II, which converts angiotensin I to angiotensin II and destroys bradykinin. Since there is no effect on ACE and there is no accumulation of bradykinin or substance P, it is unlikely that the use of angiotensin II antagonists can be associated with cough. According to the results of clinical trials where valsartan was compared with an ACE inhibitor, the incidence of dry cough was significantly lower  in patients treated with valsartan than in those treated with an ACE inhibitor. In a clinical study in patients with marked dry cough during ACE inhibitor therapy in history, the incidence of cough was 19.5% in patients treated with valsartan and 19.0% receiving thiazide diuretics, compared with 68.5% of patients who were treated with ACE inhibitor (p <0.05). Valsartan does not bind or block hormone receptors or other ion channels that are important in the regulation of the cardiovascular system.

The use of valsartan in patients with hypertension leads to a reduction of blood pressure without changes in heart rate (HR). In most patients, after administration of a single dose onset antihypertensive effect observed within 2 hours, and the maximum reduction in blood pressure is achieved within 4-6 hours and lasts for 24 hours after ingestion of the drug.
If readmission valsartan its antihypertensive effect is stabilized irrespective dose, reached after 2-4 weeks and is maintained at that level during prolonged therapy. Stop receiving valsartan is not accompanied by a sharp rise in blood pressure, or other unwanted clinical consequences. Valsartan concentration has no effect on total cholesterol, triglycerides, fasting glucose and uric acid in serum.

After myocardial infarction
in patients with acute myocardial infarction and confirmed heart failure, and / or impaired left ventricular systolic function the use of valsartan in combination therapy consisting of aspirin, beta-blockers, ACE inhibitors, thrombolytics, and HMG-CoA reductase leads to reduce mortality from cardiovascular causes after acute myocardial infarction and increase the time before the development of cardiovascular events. Reduces the incidence of hospitalizations for heart failure and myocardial infarction recurrence.

Valsartan is rapidly absorbed after oral administration, but the degree of absorption varies widely. The average value of the absolute bioavailability is 23%. Pharmacokinetic curve valsartan is downward biexponential character (half-life (T1 / 2) ɑ-phase is less than 1 hour, and (T1 / 2) β-phase of about 9 hours).
The pharmacokinetics of valsartan in the range studied doses is linear.
If readmission valsartan into changes in indicators of pharmacokinetics of the drug is not observed, and while taking the drug once a day – its accumulation is negligible.
The time required to reach maximum concentration (the C max ) -. 2:00
Plasma concentrations of valsartan are similar in men and women. Valsartan largely bound to serum proteins (94-97%), mostly to albumin. The volume of distribution at steady state is low (about 17l). . Compared to the liver blood flow (30 l / h), the plasma clearance of the drug is relatively low (about 2 L / h)
after oral administration to 83% of an oral dose of the drug is excreted through the intestines anadrol dosage and 13% – kidney, mainly unchanged form. About 20% of the dose is excreted as metabolites. The main metabolite – valeryl 4-hydroxy. The enzymes involved in the metabolism of valsartan are not defined and do not refer to the cytochrome P450 isozymes.
When taken with food valsartan decreased area under the curve, “concentration-time” (AUC) of 48%. However, after 8 hours after administration of the drug plasma concentrations of valsartan taken on an empty stomach with food and the same. Reducing AUC is not accompanied by a clinically significant decrease in the therapeutic effect, so the drug can be used both before and after a meal.

Pharmacokinetics in special patient groups Elderly Some elderly patients, systemic exposure to valsartan more pronounced when compared with patients younger age. Elderly patients is recommended to use a lower initial valsartan doses of 40 mg. Patients with renal impairment Since the renal clearance is only 30% of the total clearance in patients with impaired renal function (creatinine clearance (CC) 20-50 ml / min.) does not require dosage adjustment in patients with impaired renal function (creatinine clearance less than 20 ml / min.) it is recommended to start treatment with the 40 mg dose. Becausevalsartan degree of binding to plasma proteins is high, its elimination by hemodialysis is unlikely. Patients with hepatic impairment Approximately 70% of the dose of valsartan appears to suck through the intestine with bile, mainly in unchanged form. Valsartan does not undergo significant biotransformation, so its systemic effect is not correlated with the degree of liver dysfunction. Therefore, in patients with hepatic insufficiency nebiliarnogo origin and without cholestasis does not require changes in the dose of valsartan. In patients with biliary cirrhosis or obstruction of the biliary tract valsartan AUC increased approximately 2-fold compared with healthy volunteers.




  • Arterial hypertension.
  • In acute myocardial infarction in a combination therapy in patients with stable hemodynamics with asymptomatic left ventricular systolic dysfunction and / or heart failure to reduce mortality after myocardial infarction.Contraindications
  • Hypersensitivity to valsartan or other ingredients.
  • Pregnancy.
  • Lactation.
  • Severe hepatic impairment (on the scale of Child-Pugh score more than 9), cirrhosis of the liver, biliary tract obstruction (cholestasis).
  • Age 18 years (effectiveness and safety have been established).With caution:
    arterial hypotension; anadrol dosage hepatic insufficiency (according to Child-Pugh score of less than 9); renal insufficiency (creatinine clearance less than 20 ml / min), including patients on hemodialysis; after myocardial infarction; hyponatremia; diet with restriction of sodium intake; bilateral renal artery stenosis or stenosis of the artery to a solitary kidney; state, accompanied by a decrease in blood volume (CBV) (including diarrhea, vomiting); Patients older than 75 years.

    Pregnancy and lactation
    Use of the drug Nortivan ® during pregnancy is contraindicated.
    Renal perfusion the fetus, which depends on the development of the RAAS, begins to operate in the third trimester of pregnancy. The risk to the fetus increases when taking valsartan in the second and third trimesters. Drugs acting on the RAAS, when applied in the second and third trimester of pregnancy can cause injury and fetal death. There are reports of spontaneous abortions, water shortages and violations of newborn renal dysfunction when pregnant women took valsartan.
    The data on the allocation of valsartan in breast milk are not available. The appointment of the drug Nortivan ® during lactation, breast-feeding should be discontinued.

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