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Ca2+ plays a vital role in the control of contractile function of vascular smooth muscle. A change in Ca2+-handling by vascular muscle may explain some altered functions associated with hypertension. This article summarizes the methodologies and their limitations in the studies of how Ca2+ is made available and then removed in the excitation-contraction-relaxation processes. A direct approach using isolated subcellular membranes in the studies of Ca2+-binding and transmembrane movement is described along with insights derived from it into the pathophysiological mechanisms of hypertension.
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