Calcium metabolism and the renin-aldosterone system in essential hypertension.

Despite recent appreciation of a role for calcium in clinical hypertension, evidence at present is conflicting. Thus, certain studies suggest increased calcium availability may be associated with increased levels of blood pressure, while others suggest that a calcium deficiency may contribute to the pathogenesis of hypertensive disease. Our own group has thus far demonstrated deviations of circulating levels of ionized calcium and of magnesium in essential hypertension, linked with concurrent deviations in the activity of the renal pressor hormone, renin. Furthermore, calcium metabolic indices may predict and even determine dietary sodium sensitivity in hypertension, as well as the blood pressure responsiveness to antihypertensive drug therapy. Moreover, oral calcium supplementation may itself possess antihypertensive actions in specifically targeted renin subgroups of essential hypertensive subjects. Altogether, these results link calcium metabolism, renin system activity, and the pathogenesis of hypertensive disease. It may ultimately be calcium-regulating hormones, which determine cellular disposition of calcium, rather than circulating levels of calcium itself, that mediate the blood pressure and possibly even the renin deviations observed among differing hypertensive individuals.