Angina pectoris results from an imbalance between the oxygen supply and the oxygen needs of the myocardium. While the classic form of angina is usually caused by demands exceeding supply, a primary and transient decrease in coronary blood flow is more and more often recognised as an aetiological factor of myocardial ischaemia. Calcium antagonists, although new in cardiovascular therapeutics, are already recognised as the treatment of choice for some forms of angina and as useful therapeutic adjuncts in others. Few contraindications to their use exist. They are potent vasodilators and they can prevent the occurrence of coronary artery spasm responsible for the Prinzmetal's variant form of angina. They can also reduce coronary artery tone, which if high, can compromise flow through a narrowed coronary artery. Nifedipine, diltiazem and verapamil can also influence the various determinants of myocardial oxygen consumption to reduce myocardial oxygen needs. Their effects on heart rate, blood pressure and on the inotropic state of the left ventricle is, in vivo, the balance between their direct effects on the vascular wall and myocardial muscular cells and their indirect effects represented by the reflex physiological responses. Significant variations in these effects exist between the 3 calcium antagonists such that treatment can be individualised to a particular patient's needs. Precautions with their use as well as most of their side effects can be understood from a knowledge of their direct and indirect properties. Other pharmacological effects of these drugs include a regional redistribution of coronary blood flow, cardioprotection, delay in cell death and possibly in the progression of atherosclerosis. The clinical significance of these properties remains to be investigated.