The thesis that primary disturbances of divalent ion metabolism contribute to the development and maintenance of hypertension is addressed. Representative interactions of calcium, magnesium, and phosphorus with normal cardiovascular physiology are presented. Established and postulated abnormalities of divalent ion metabolism associated with human and experimental hypertension are reviewed. The influence of calcium balance on blood pressure development in the young spontaneously hypertensive rat is demonstrated by the results of a diet intervention study. Twelve male SHRs were randomized at 4 weeks of age to one of three diets that differed only in the calcium content (0.25%, 0.5%, and 4.0% by weight). The SHRs' blood pressures stratified inversely (p less than 0.001) based upon the calcium content. The low calcium animals experienced a more rapid and greater rise in blood pressure between 4 and 20 weeks of age (p less than 0.01). Blood pressures of the supplemented SHRs (4%) peaked at a lower value (174 vs 192 mm Hg, p less than 0.01). After maturity, the 4% SHRs experienced an attenuation (p less than 0.01) of their hypertension (154 +/- 7 mm Hg, 4% SHR vs 176 +/- 7 mm Hg, 0.5% SHR). It is proposed that membrane-associated bioavailable Ca2+ is reduced in the SHR, and possibly in human, hypertension. Dietary calcium supplementation may reverse this defect, resulting in cell membrane stabilization and vascular smooth muscle relaxation.