Calcium in the pathogenesis and therapy of human hypertension.

The contribution of calcium to normal regulation of blood pressure is reviewed. Epidemiologic data suggest that abnormal calcium homeostasis may play a role in dietary and environmental contributions to the risk of hypertension and cardiovascular disease. Recent studies in human and experimental hypertension point to one or more defects in cellular handling of calcium as contributing to the initiation and maintenance of increased vascular tone and, thereby, to abnormally elevated arterial blood pressure. By "correcting" some of these defects, calcium channel blockers may represent relatively specific therapy for hypertension. Data from human trials are still limited, but it is evident that, following oral administration of nifedipine and related compounds, an immediate decrease in peripheral vascular resistance and mean arterial pressure is produced. Cardiac output is not altered, and renal perfusion is maintained. In contrast to many currently used antihypertensive agents--including thiazide diuretics and beta blockers--which frequently induce alterations in the patient's serum chemical values, long-term administration of calcium channel blockers does not produce significant adverse metabolic effects or substantive changes in biochemical parameters.