Mode of Action of Beta Blockers in Angina Pectoris

Abstract

The therapeutic effect of beta adrenoceptor blockers in angina pectoris can be ascribed to an inhibition of beta1 receptor mediated stimulation of heart rate and myocardial contractility, resulting in an improved oxygen supply-demand balance in the myocardium. When given in equipotent beta1 blocking doses, the nonselective blocker propranolol and the beta1 selective blocker metoprolol differ markedly as regards inhibition of adrenaline induced beta2 mediated vasodilatation. Only propranolol will inhibit this effect. After propranolol, adrenaline therefore elicits a haemodynamic effect pattern characterized by high peripheral vascular resistance, high arterial blood pressure, low cardiac output and increased cardiac size. In view of these findings it is suggested that a beta1 selective blocker may be a more efficient antianginal agent than a nonselective blocker in those patients in which the anginal attack is associated with a significant release of adrenaline. The clinical relevance of this hypothesis has not been tested.

Do beta adrenoceptor blocking agents provide the same degree of clinically convincing morbidity and mortality benefits in patients with chronic heart failure? A literature review

“…However, recent scienti ic evidences suggest that they are no longer preferred irst choice for the initial management of hypertension in most patients [22]. In daily clinical practice, it is acceptable to use Therapeutic bene its of beta adrenoceptor blocking agents in Cardiac arrhythmias: The anti-arrhythmic effects of beta adrenoceptor blocking agents are generally as a result of their direct cardiac electrophysiological actions that include: reduced heart rate, decreased spontaneous ectopic pacemakers, slowed conduction and increased refractory period of the Atrioventricular (AV) node [23,24].…”