Hyposart, tablets 8 mg 28 pcs.

Angiotensin II receptor antagonist. Angiotensin II is the main enzyme of the RAAS, involved in the pathogenesis of arterial hypertension, heart failure and other cardiovascular diseases.

Candesartan is a selective angiotensin II receptor antagonist of subtype 1 (AT1-receptors). It does not exhibit agonist properties (does not affect ACE and does not lead to accumulation of bradykinin or substance P, does not bind to receptors of other hormones, does not affect ion channels involved in the regulation of cardiovascular system activity). As a result of blocking of AT1-receptors of angiotensin II there is a compensatory dose-dependent increase of renin activity, concentration of angiotensin I, angiotensin II and decrease of plasma concentration of aldosterone.

Arterial hypertension Oral administration of candesartan provides a dose-dependent, smooth decrease in BP by reducing PPS without a reflex increase in HR. There are no data on the development of significant arterial hypotension after the first dose or on the development of withdrawal syndrome after discontinuation of therapy.

The onset of antihypertensive action after the first dose of the drug usually develops within 2 hours, the duration of effect is 24 hours. Against the background of continuing therapy with candesartan in a fixed dose, maximum BP reduction is usually achieved within 4 weeks and is maintained throughout treatment.

The addition of the thiazide diuretic hydrochlorothiazide to candesartan enhances its antihypertensive effect. The patient’s age and gender have no effect on the efficacy of the drug. Candesartan increases renal blood flow and does not alter or increase glomerular filtration rate, whereas renal vascular resistance and filtration fraction decrease.

Candesartan has a less pronounced antihypertensive effect in patients of non-hypertensive race (a population with predominantly low plasma renin activity).

There are no data on the effect of candesartan on the progression of diabetic nephropathy. In patients with arterial hypertension and type 2 diabetes mellitus, candesartan has no adverse effect on blood glucose concentration and lipid profile. Heart failure therapy with candesartan reduces mortality rate and hospitalization rate in patients with chronic heart failure (CHF) regardless of age, sex and concomitant therapy, leads to a decrease in functional class of CHF by NYHA classification.

Candesartan is effective in patients taking simultaneously beta-adrenoblockers in combination with ACE inhibitors; its effectiveness is independent of the ACE inhibitor dose. In patients with CHF and reduced left ventricular systolic function (left ventricular ejection fraction (LVEF) less than 40%), candesartan reduces PEEP and congestion pressure in the pulmonary capillaries.

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