An Official Journal of the American Heart Association

The experimental design which most closely reproduces clinical renovascular hypertension is constriction of one renal artery, with the other renal artery and kidney left intact. To test the role of renin and angiotensin in the pathogenesis of renovascular hypertension, attempts were made to induce such hypertension in rats previously immunized with angiotensin. In 29 highly immunized and 33 control rats, one renal artery was partially constricted and the other kidney and renal artery left intact. Preoperative blood pressures were equal in all rats (means: immunized, 118 ± SE 0.95; controls, 117 ± 0.70 mm Hg). Both groups developed hypertension during the 13 days following operation (means: immunized, 173 ± 3.42; controls, 169 ± 4.65 mm Hg). The high blood pressures persisted throughout the observation period (56 days). Immune sera completely inactivated large amounts of angiotensin (mean, 1130 ± SD 887 ng/ml antiserum; range 200—4000), and high intravenous doses of renin and angiotensin had no effect on the blood pressure of immunized rats. These data provide strong evidence that the direct pressor effect of circulating angiotensin is not essential for the development of hypertension evoked by constricting one renal artery in the rat.