Hypertension, Vol 7, 607-627, Copyright © 1985 by American Heart Association
DA McCarron
The hypothesis that abnormalities of calcium homeostasis at both an organ
and cellular level are a primary factor in the pathogenesis of human and
experimental hypertension forms the basis of this review. The rapidly
expanding data base relating disordered calcium metabolism to altered
vascular smooth muscle function and increased peripheral vascular
resistance is summarized and integrated with the observations that reduced
dietary calcium intake is the most consistent nutritional correlate of
hypertension in the United States. The role of sodium and sodium chloride
in pathogenesis of hypertension is reassessed in the light of new data from
epidemiological clinical research, experimental models, and cell physiology
investigations. The data supporting the thesis that the effects of sodium
or chloride or both on blood pressure may represent, in selected
situations, secondary influences mediated through induced changes in
calcium homeostasis are presented. The interface between these nutritional
factors and the normal regulation of vascular smooth muscle is discussed,
providing a theoretical framework in which to assess the current
information and to formulate the necessary future research.
ARTICLES
Is calcium more important than sodium in the pathogenesis of essential hypertension?
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