A major focus of past and recent research in hypertension has been on the characterization of the nature of the vasculature changes which lead to the observed increase in total peripheral resistance responsible for the elevation of arterial pressure. Here we survey recent evidence which suggests that altered handling of calcium is a primary membrane defect in hypertension. Evidence for the primacy of this defect is provided by studies demonstrating a reduced ability of the membrane to bind calcium in diverse tissues from hypertensive animals. The reduced calcium binding ability appears to be responsible for a greater membrane permeability to monovalent and divalent cations. This greater permeability contributes to the increased sensitivity to vasoconstrictor stimuli of vascular smooth muscle in hypertension.
|Original language||English (US)|
|Number of pages||19|
|Journal||Progress in clinical and biological research|
|State||Published - Jan 1 1986|
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