This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dustan, H. P. Articles by Kirk, K. A. Search for Related Content PubMed PubMed Citation Articles by Dustan, H. P. Articles by Kirk, K. A.

Hypertension, Vol 13, 696-705, Copyright © 1989 by American Heart Association

ARTICLES

Corcoran lecture: the case for or against salt in hypertension. Arthur Curtis Corcoran, MD (1909-1965). Tribute and prelude to Corcoran Lecture of 1988

HP Dustan and KA Kirk
Department of Medicine, University of Alabama, Birmingham.

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.

This article has been cited by other articles:

				O. Schmidlin, A. Forman, M. Tanaka, A. Sebastian, and R. C. Morris Jr NaCl-Induced Renal Vasoconstriction in Salt-Sensitive African Americans : Antipressor and Hemodynamic Effects of Potassium Bicarbonate Hypertension, February 1, 1999; 33(2): 633 - 639. [Abstract] [Full Text] [PDF]

				M. M. E. Krekels, N. C. Schaper, and P. W. de Leeuw Sensitivity of Blood Pressure and Renin Activation During Sodium Restriction Hypertension, November 1, 1997; 30(5): 1216 - 1222. [Abstract] [Full Text]

				M. H. Weinberger Salt Sensitivity of Blood Pressure in Humans Hypertension, March 1, 1996; 27(3): 481 - 490. [Abstract] [Full Text]

				P. van Paassen, D. de Zeeuw, G. Navis, and P. E. de Jong Does the Renin-Angiotensin System Determine the Renal and Systemic Hemodynamic Response to Sodium in Patients With Essential Hypertension? Hypertension, February 1, 1996; 27(2): 202 - 208. [Abstract] [Full Text]