The role of renin in experimental hypertension

Abstract

In 1934 Goldblatt and others discovered that partial constriction of the main renal artery produces a marked and permanent hypertension in the dog. The renal experimental hypertension caused by this or other methods in laboratory animals is similar in many respects to human essential hypertension. It is not due to excretory insufficiency of the kidney or to an increase of blood volume or cardiac output, nor is it produced through a nervous mechanism. Houssay and Fasciolo (1937a, 1937b) have shown that renal ischaemia results in hypertension through a humoral mechanism. The ischaemic kidneys of dogs with chronic hypertension were grafted into the neck of normal or nephrectomized dogs. The arterial pressure of the recipient dog rose from 30 to 80 mm. Hg in 5 to 10 minutes, while grafting a normal kidney had no such effect. The citrated plasma obtained from the veins of these ischaemic kidneys produced vasoconstriction when perfused through a Lawen-Trendelenburg preparation; normal plasma had no vasoconstrictor action (Houssay and Taquini, 1938