Abstract
Theoretical mechanisms underlying dietary calcium's antihypertensive action are reviewed. Based upon known defects in the regulation of membrane Ca2+ transport and regulation of intracellular free Ca2+ concentration, we conclude that maneuvers that favorably modify calcium homeostasis such as dietary calcium supplementation or 1,25 (OH)2 vitamin D3 administration appear to favorably modify these defects. Consequent improvements in vascular smooth muscle function may mediate the reductions in blood pressure that follows chronic dietary calcium supplementation in experimental hypertension and in the clinical setting.
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