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CALCIUM ANTAGONISTS AND GLYCAEMIC CONTROL

Calcium antagonist drugs are increasingly being recognized as major therapeutic agents in the treatment of cardiovascular disease. Although their chemical structures vary widely they seem to have similar, though not identical, modes of action. Their roles in the management of angina (1, 2), hypertension (3, 4) and supraventricular tachyarrhythmias are well established (5). Their potential efficacy in hypertrophic obstructive cardiomyopathy (6), in heart failure (7) and as cardioprotective agents (8) is currently under review. The three agents in widespread clinical use are nifedipine, verapamil and diltiazem. Nifedipine has been used most extensively in the Western World and is predominantly a peripheral arterial vasodilator (9, 10). Verapamil has been in clinical use for the longest period of time and has an undisputed reputation in the treatment of supraventricular tachycardia ( 5 ) . Perhaps unfortunately its effects on the A-V node have distracted clinicians from appreciating its efficacy in the management of angina (2) and hypertension (1 1). Diltiazem is the most recent arrival in the U.K. but has been extensively used for many years in Japan. Its particular therapeutic use, to date, has been in the control of angina ( 12, 13). The major unwanted effects of calcium antagonists: headaches, postural hypotension, flushing and oedema are probably caused by vasodilatation. However, in common with thiazide diuretics (1 4) and beta adrenergic blockers (1 5) concern has been raised over their effects on glycaemic control. The potential for an influence of calcium antagonists upon carbohydrate homeostasis is great, in view of the many calcium-dependent processes involved. Grodsky and Bennett (1 6), and subsequently others (17, 18), have demonstrated that glucose-induced insulin secretion is a calcium dependent process. In addition, alpha-adrenergic receptor-mediated glycogenolysis has been shown to operate through calcium release from intra-mitochondria1 pools (19). The influence of calcium on these processes and the other actions of calcium antagonists on intracellular metabolism mean that the range of processes that may be susceptible to influence by these drugs is large. Abnormalities in glucose tolerance are particularly common in patients with hypertension and angina (20). Furthermore, diabetes mellitus is an important risk factor in coronary artery disease. It is, therefore, important to know what effects drugs used in these ‘at risk’ patients will have on blood sugar control. The aim of this article is to review the known effects of the three more commonly used calcium antagonists on glucose metabolism, and to discuss the relevance of these effects in the clinical situation.