THE RÔLE OF RENAL METABOLISM IN HYPERTENSION AND UREMIA

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Abstract
Expts. were conducted in which ureter-vein anastomosis were made on a non-ischemic kidney and thereafter the immediate effect of nephrectomy of the contralateral was observed. The time for the dissipation of the existing hypertension was noted and was the same as in previous expts. in which the normal kidney was left in situ. However, the blood N P N, rose. The chemical mediator of renal hypertension was evidently rapidly destroyed by the metabolic activity of the normal kidney. The excretory function of the kidney played little role in eliminating the mediator. If specific substances were responsible for the uremic syndrome, they were 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. No evidence was obtained to support the view that a unilateral uretero-venous fistula led to nephrotoxic symptoms.

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