Renal Transplantation Study of Infarcted Kidney as Carriers of a Hypertensive Factor in the Rat

Hypertension, produced in rats by unilateral nephrectomy and partial infarction of the remaining kidney, was transferred to recipient isogeneic rats so long as the kidney was transplanted within 12 days after infarction. After a week, the renin content of the transplanted infarcted kidneys was approximately one-third of that in control animals, indicating that the hypertension probably was not renin-related. Removal of the infarcted kidney and transplantation of an isogeneic normal kidney uniformly rendered previously hypertensive rats normotensive, while rats receiving a normal kidney without removal of the infarcted kidney remained hypertensive. Since the transplanted kidney is totally denervated and has a grossly reduced renin content, the hypertension of renal infarction is presumed to be the result of a humoral agent or agents other than renin. The low renin titer found by others in chemically or surgically denervated kidneys was found also in normal isografted and rejecting allografted kidneys, confirming the previously described contribution of the renal sympathetic nerve supply to renin production. The failure of infarcted kidneys to induce hypertension in isogeneic recipients when transplanted 2 weeks or more after infarction is unexplained.