Corcoran lecture: the case for or against salt in hypertension. Arthur Curtis Corcoran, MD (1909-1965). Tribute and prelude to Corcoran Lecture of 1988.
Salt intake in excess of body needs has long been considered a factor in the genesis and maintenance of human hypertension; the mechanism is salt retention due to faulty renal excretory efficiency. This discussion reviews clinical studies that make a case either for or against the salt hypothesis. Included is a summary of recent experiences with 4 days of salt depletion and 3 days of salt loading in 96 normotensive control subjects and 40 hypertensive patients. These studies were done to test the hypothesis that salt-sensitive blood pressure changes are quantitatively related to sodium balance. However, we found no statistically significant relation between arterial pressure changes and sodium lost during salt depletion or retained during salt loading. The failure of that hypothesis prompted a study of the known factors that control arterial pressure by using multidimensional response surface modeling for changes produced by salt loading. The analysis indicated that in these experiments salt-sensitive blood pressure changes of hypertensive patients were controlled differently than those of normotensive subjects. In the hypertensive group, the changes were highly predictable by combinations of variables, which featured plasma aldosterone, norepinephrine, and epinephrine. In the normotensive group, the changes were less predictable; fewer of the factors were involved, and plasma renin activity was the featured variable. These findings and results of studies done over the past 50 years indicate that salt-dependent hypertension is controlled by many factors and is not a strict correlate of salt intake.
Dustan
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Department of Medicine, University of Alabama, Birmingham.
Kirk
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D000450:Aldosterone / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000139:chemically induced*; D012964:Sodium / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology
D012965:Sodium Chloride; D000450:Aldosterone; D012964:Sodium