There is no doubt that calcium antagonists are effective antihypertensive agents. Their antihypertensive potency is comparable with that of beta-blockers and angiotensin-converting enzyme inhibitors. Blood pressure decreases are dose dependent with no orthostatic reactions, and are more pronounced in patients with lower renin levels, which is demonstrable in both white and black patients; whether the blood pressure response is stronger in elderly patients remains to be ascertained. Blood pressure rises during stress are moderately decreased. Basic documentation has been obtained for first-generation calcium antagonists, and the newer members of this class of drugs--nearly all dihydropyridine derivatives--were developed to achieve greater vascular specificity and a longer duration of action. With calcium antagonists, blood pressure decreases are due to decreases in peripheral resistance. However, blood flow increases do not necessarily persist over time, thus raising the question of what is the mechanism for the long-term decreases in blood pressure. Several studies have shown that blood pressure variability is unchanged with calcium antagonists. However, blood pressure decreases are accompanied by regression of left ventricular hypertrophy, which is understandable in light of the strong correlation between parathyroid hormone and left ventricular hypertrophy. The use of calcium antagonists in the treatment of clinical hypertension can be guided by the following facts: 1) They are metabolically neutral and are accompanied by few or no life-threatening side effects that, when they do occur, tend to disappear over time; 2) They increase blood flow to muscle and help control angina pectoris as well as vasospastic diseases.