Effects of Chronic Excess Salt Ingestion: Lack of Gross Salt Retention in Salt-Hypertension. ()

Abstract

Conclusion These studies on experimental hypertension are not in agreement with our clinical research (1,2) in which there was evidence that the biological half-life (T_½) of ²²Na often was prolonged in patients with uncomplicated essential hypertension. The present work on rats from 2 inbred strains having opposite genetic susceptibilities to hypertension induced by salt suggested the contrary: the biological T_½ of ²²Na was found to be shorter in the strain predisposed to hypertension, and did not appear to be related to elevations in blood pressure, per se. Tissue sodium was not found to be increased in animals with hypertension, nor was there evidence of potassium depletion. It is possible that the shorter biological T_½ of ²²Na in the group predisposed to hypertension was due to a slightly greater food (i.e., NaCl) intake as compared with the animals resistant to the development of hypertension. In sum, this evidence strongly suggests that however excess salt ingestion induces hypertension, it is not through gross accumulation of sodium, or depletion of potassium, in tissues. However, by the techniques used here, focal accumulation, e.g., in arterioles(21), would not have been found.