Abstract

Verapamil (Cordilox - Pfizer; iproveratril*), described by the manufacturers as a mild beta-blocking agent, is promoted as an important new compound for the long-term control of angina pectoris.¹ It is claimed that, unlike other beta-blocking agents which reduce the response of the heart to sympathetic stimulation, verapamil induces neither coronary vasoconstriction nor broncho-spasm and is less likely to provoke low-output cardiac failure. These unwanted effects are an unavoidable consequence of intense beta receptor blockade, and (although the manufacturers attribute the advantages to a direct relaxation of plain muscle) their absence suggests that the action of verapamil may depend not on beta receptor blockade but on other mechanisms. The claims for verapamil of advantages over potent beta-blocking agents are clearly aimed at propranolol (Inderal - ICI), the only one available for clinical use. We discussed propranolol in 1965.¹