Calcium as a Mediator of Salt Sensitive Hypertension

Abstract

Dietary salt intake has long been recognized as a factor in clinical and experimental hypertensive disease. However, when attention remains narrowly focused on salt and/or sodium alone, the mechanism(s) by which increases in dietary, extracellular, or intracellular sodium lead to increases in blood pressure, still remain unclear. Increased tissue and presumably intracellular sequestration of sodium was initially observed by Tobian (1), accounted for prhps by now widely postulated circulating inhibitors of Na⁺ -K⁺ -ATPase, stimulated by the volume expansion of salt loading in salt sensitive hypertensive animals and humans (2). Linking calcium with sodium has led to a further understanding of salt-induced hypertension. Calcium is required as a final common mediator of smooth muscle contraction, and thus of peripheral vasoconstrictor tone, characteristically elevated in human hypertension (3). Parallel studies over the past three decades have also demonstrated the sodium dependence of cellular calcium uptake in arterial smooth muscle (4). This led to the much discussed hypothesis by which this sodium-calcium exchange mechanism may be involved in human hypertension (5).