THE LIVER is well known for its ability to metabolize endogenous substances. Its possible role in modulating the pressor substance released by the ischemic kidney was first investigated by Child and Glenn1 in 1938. These authors concluded that the diversion of venous blood from the ischemic kidneys into the liver did not effect the elevated blood pressure. In the same year Levy and Blalock2 reported on the ineffectiveness of such diversion in preventing the development of hypertension when the artery to the only remaining kidney was later constricted.
This aspect of experimental renal hypertension remained dormant until 1962 when Aoki3 reported on the effectiveness of renalportal venous shunt in restoring normotensive condition in the hypertensive dog and preventing the development of hypertension due to subsequent renal-artery constriction. He related this to the detoxifying ability of the liver.
In an attempt to find an explanation for these contradictory