PMID: 6113811Oct 1, 1980Paper

Clinical pharmacology of beta-adrenoceptor antagonism in angina pectoris: an overview

Annals of the Academy of Medicine, Singapore
V M Oh

Abstract

Beta antagonists competitively block beta 1-adrenoceptors that mediate both the rate and force of myocardial contraction. Their precise mechanism of anti-anginal action is uncertain. A reduction in oxygen demand may relative pain and improve effort tolerance. Alternatively inhibition of the adrenergic drive to contraction may offset the increased ventricular wall tension due to incomplete relaxation. Partial agonist activity in a beta-antagonist does not influence efficacy nor protect against airflow obstruction. Membrane stabilising activity is clinically trivial. Cardioselectivity makes airflow obstruction less likely at low but not at high blood concentrations of drug. Alpha-receptor antagonism may also prevent broncho-constriction; it has not been assessed in coronary vasospasm. The dosage and choice of drugs are based on pharmaco-kinetic and dynamic data in animals and man. The major side-effects of beta-blockade are heart failure and airflow obstruction. Cardiotoxicity from overdosage may be treated with isoprenaline, dopamine or glucagon while beta 2-agonists will reverse bronchoconstriction. Since beta-antagonists raise-peripheral vascular impedance, reduction of preload with nitrates enhances their antianginal efficacy...Continue Reading

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