Correlation of the Pressor Activity of the Renal Venous Effluent with Excretory Function and Other Tests in Focal, Parenchymal, and Vascular Renal Disease

Abstract

A series of 170 hypertensive patients suspected of suffering from renovascular disease have been subjected to various tests designed to identify the presence of a surgically remediable lesion. The presence of a pressor agent in the renal venous effluent, as determined by bioassay on the rat, has proven to be an accurate method for detecting the presence of renovascular hypertension responsive to surgical treatment. Split-function excretory tests, aortography, and other tests used for this purpose could not be relied on as the sole criterion as to whether surgical intervention is indicated in a given patient.

Differentiation of Nephrotensin from Angiotensin I and II

“…Prepossession with renin has led to the assumption that this pressor agent is angiotensin 11. In previous reports from this laboratory (4,6), it has been shown, however, that a hitherto unrecognized pressor agent is formed in ischemic renal tissue and that it is this agent which is responsible for the elevation in blood pressure in so-called "renovascular" (more accurately designated as surgically remediable) and in acute experimental hypertension. Nephrotensin, as this pressor agent has been designated has been claimed to be identical or immunologically related to angiotensin I (7) but incubation with angiotensin I antibody makes it possible to differentiate them.…”

“…I t is well established that experimental hypertension induced acutely by drastic restriction of the renal artery and rare instances of hypertensive disease in, the human differ in several fundamental respects from chronic sustained hypertensive disease (1)(2)(3)(4)(5). Only in the former is the elevation in blood pressure alleviated by nephrectomy and is the presence of a pressor agent demonstrable in the renal venous effluent from the affected kidney (3,5).…”

“…That the acute elevation in blood pressure observed following drastic restriction of the renal artery and in surgically remediable hypertension of the human differ pathogenetically from the elevation observed in the chronic stage of hypertensive disease is apparent from the fact that only the former are relieved by nephrectomy and are accompanied by the presence in the renal venous effluent of a demonstrable pressor agent (1)(2)(3)(4)(5). The results of the present study support the claim that nephrotensin, a newly described pressor agent, and not angiotensins I or I1 resulting from an excessive production of renin by the ischemic kidney is responsible for the observed rise in blood pressure in acute and surgically remediable hyper tension.…”