Calcium channel function in hypertension

Abstract

Calcium channel function is fundamental to membrane excitation in vascular muscle, and imparts the notable voltage sensitivity to small blood vessels. The actions of the electrogenic sodium pump on membrane potential, and thus calcium channels, can explain perturbations that could alternately be conceived as acting on other mechanisms. Evidence for altered calcium channel function in hypertension suggests that deficiencies in function of the calcium channel per se lie at the root of altered membrane function. In this respect the disease may be similar to at least one form of skeletal muscle dysgenesis. Proportional increases in BP and Ca2+ current in vascular muscle of stroke-prone genetically hypertensive rats further strengthen this hypothesis of altered Ca2+ channel function in hypertension. Increased calcium in the subsarcolemmal space and several recently discovered substances that may endogenously modulate Ca2+ channels are additional evidence for abnormal Ca2+ channel function in BP regulation. From several kinds of evidence and multiple investigators, it is reasonable to conclude that calcium channel malfunction plays an important role in the vascular muscle contribution to hypertension.