The Rôle of Renal Metabolism in Hypertension and Uremia

Abstract

1. The chemical mediator of renal hypertension is rapidly destroyed by the metabolic activity of the normal kidney. The excretory function of the kidney plays little, if any, rôle in eliminating the mediator of hypertension. 2. If specific substances are responsible for the uremic syndrome, they are neither produced nor eliminated to any significant extent by the metabolic activity of the kidneys. The elimination of these postulated uremia-producing substances would have to be primarily dependent upon the excretory activities of the kidney. 3. No evidence was obtained to support the view that a unilateral ureterovenous fistula leads to "nephrotoxic" symptoms.

The Effect of High Protein Diets on Experimental Renal Hypertension

“…Although the processes which result in relative renal excretory insufficiency and those factors which lead to hypertension are frequently seen together, we have shown that they are fundamentally distinct (14,15). Nevertheless there still remains the possibility that an augmented load on the kidney might cause an increased amount of work and thus lead to a relative renal ischemia and the induction of those processes which lead to hypertension.…”

“…Others have maintained that the amount of protein in the diet generally has little or no relation to the blood pressure (6, 7). It has even been suggested that a continued low protein diet may be pathogenic (8,9).The relationships between renal excretory insufficiency and diet have been studied experimentally by numerous investigators (10), but the recent development of a satisfactory method for the experimental production of persistent renal hypertension (11) has made possible studies on the relationship between the factors of diet, renal excretory insufficiency and hypertension of renal origin in animals (12,13).Although the processes which result in relative renal excretory insufficiency and those factors which lead to hypertension are frequently seen together, we have shown that they are fundamentally distinct (14,15). Nevertheless there still remains the possibility that an augmented load on the kidney might cause an increased amount of work and thus lead to a relative renal ischemia and the induction of those processes which lead to hypertension.…”

The Pathogenesis of Hypertension Induced by Renal Constriction

“…In general, after unilateral operative procedures and in the presence of unilateral renal disease hypertension does not develop, although there may be exceptions to this rule. There is evidence that it is due to inactivation of a pressor substance by the intact kidney (23). Only in this limited sense does the contention of Grollman seem valid.…”