Abnormalities of membrane transport in hypertension.

In this review, postulated passive and active fluxes of sodium, potassium, and calcium across the sarcolemma of the normal vascular smooth muscle cell are first summarized. Some practical problems encountered in their measurement are also mentioned. The review then considers how these fluxes appear to be altered in various forms of hypertension in animals and humans. Emphasis is given to abnormal fluxes of sodium and potassium due to altered sodium pump activity and permeability. Increasing evidence indicates that sodium retention due to increased sodium intake or decreased sodium excretion causes hypertension by releasing a humoral pressor substance from brain. This substance, which may be the putative natriuretic hormone, inhibits Na+, K+-ATPase and sodium pump activities in blood vessels and heart, thereby increasing contractile activity. In the genetic models of hypertension, the primary defect appears to be increased permeability of the vascular smooth muscle cell wall to sodium; pump activity increases to compensate for the increased inward leak of sodium. This may also be the case in patients with heritable essential hypertension. The possible consequences of super-imposing the sodium pump inhibitor on the primary defect are also considered. This may occur when animals with genetic hypertension or patients with heritable essential hypertension retain sodium subsequent to increased sodium intake and/or decreased ability to excrete sodium. Such superimposition should raise intracellular sodium concentration to high levels since now the pump would not fully compensate for the increased inward leak of sodium.