Biscore 2.5/Biscore 5 Mechanism of Action

Pharmacology: Bisoprolol is a potent highly beta₁-selective-adrenoceptor blocking agent, lacking intrinsic stimulating and without relevant membrane stabilizing activity. It only shows low affinity to the beta₂-receptor of the smooth muscles of bronchi and vessels as well as to the beta₂-receptors concerned with metabolic regulation. Therefore, Bisoprolol is generally not to be expected to influence the airway resistance and beta₂-mediated metabolic effects. Its beta₁-selectivity extends beyond the therapeutic dose range.
Hypertension or angina pectoris: Bisoprolol is used for the treatment of hypertension and angina pectoris. As with other Beta₁-blocking agents, the method of acting in hypertension is unclear. However, it is known that Bisoprolol reduces plasma renin activity markedly.
Antianginal mechanism: Bisoprolol by inhibiting the cardiac beta receptors inhibits the response given to sympathetic activation.
That results in the decrease of heart rate and contractility this way decreasing the oxygen demand of the cardiac muscle.
In acute administration in patients with coronary heart disease without chronic heart failure Bisoprolol reduces the heart rate and stroke volume and thus the cardiac output and oxygen consumption. In chronic administration the initially elevated peripheral resistance decreases.
Pharmacokinetics: Bisoprolol is absorbed almost completely from the gastrointestinal tract. Together with the very small first pass effect in the liver, this results in a high bioavailability of approximately 90%. The plasma protein binding of Bisoprolol is about 30%. The distribution volume is 3.5 L/Kg. The total clearance is approximately 15 L/h.
The plasma elimination half-life (10-12 hours) provides 24 hours efficacy following a once daily dosage.
Bisoprolol is excreted from the body by two routes, 50% is metabolized by the liver to inactive metabolites which are then excreted by the kidneys. The remaining 50% is excreted by the kidneys in an unmetabolized form. Since elimination takes place in the kidneys and the liver to the same extent a dosage adjustment is not required for patients with impaired liver function or renal insufficiency.