MECHANISMS OF DESOXYCORTICOSTERONE ACTION. II. RELATION OF SODIUM CHLORIDE INTAKE TO FLUID EXCHANGE, PRESSOR EFFECTS AND SURVIVAL

Abstract

Increased Na intake in rats up to 2% of body wt. per day was accompanied by elevation of fluid exchange, increased heart and kidney wt. and reduction in growth rate, but did not provoke hypertension. The data indicate that increased velocity of fluid exchange represents a mechanism for augmenting the renal excretion of Na, even under circumstances in which the increase in velocity entails further intake of a salt-containing soln. The primary effect of DCA was to elevate the level of fluid exchange over control values by a ratio fixed by the dose of the drug and the amt. of supplementary salt admn. Hypertension was a subsequent development. The magnitude of DCA-induced hypertension did not correlate with the level of salt exchange, although it was augmented by salt admn., particularly at low DCA dosage levels. The effects of salt supplementation of DCA-implants on heart and kidney wt. and on survival were disproportionate to the measured augmentation of blood-pressure elevation. The resemblance between the action of salt in the DCA-induced hypertension of animals to that in essential hypertension lends additional support to the hypothesis that the mechanism of sustained pressure elevation in the human involves increased activity of the adrenal cortex. The favorable survival time of DCA-treated animals, once the period of most intense drug action had been passed, suggests the possibility of arresting human hypertensive disease either by removal of the adrenal cortex or by nullification of the activity of its salt-retaining steroids.