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Selective beta1-adrenoblocker without intrinsic sympathomimetic activity, does not have membrane-stabilizing effect. Bisoprolol in therapeutic doses has low affinity to beta2-adrenoreceptors of internal organs (pancreas, skeletal muscles, smooth muscle of peripheral arteries, bronchi and uterus), as well as to beta2-adrenoreceptors involved in the regulation of metabolism. Consequently, bisoprolol (unlike non-selective beta-adrenoblockers) in general does not affect airway resistance, has a less pronounced effect on organs containing beta2-adrenoreceptors, and on carbohydrate metabolism, does not cause sodium ion retention in the body. The severity of atherogenic effect of bisoprolol does not differ from that of propranolol. In therapeutic doses bisoprolol blocks beta1-adrenoreceptors of heart, reduces catecholamine-stimulated formation of cAMP from ATP, reduces intracellular calcium ion current, has negative chrono-, dromo-, batmo- and not obviously expressed inotropic effect. Bisoprolol reduces heart rate (HR) at rest and on exertion, slows atrioventricular conduction, reduces myocardial excitability. Reduces cardiac output, reduces stroke volume to a small extent. Reduces myocardial oxygen demand, reduces plasma renin activity.

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LLC Pharmasyntez-Tyumen

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