SLOW PRESSOR EFFECT OF ANGIOTENSIN-II IN NORMOTENSIVE RATS WITH RENAL-ARTERY STENOSIS

1. We have shown previously that renal artery stenosis in rats causes enhanced responsiveness to the slow presser effect of angiotensin II ( AngII) and suggested that two-kidney, one clip (2K1C) hypertension may depend, in part, on changes in responsiveness to the peptide. 2. The present experiment was performed in order to investigate whether a deg ree of renal artery stenosis that was insufficient to raise blood pres sure was able to enhance responsiveness to the slow presser effect of AngII. 3. Two to four weeks after placement of a 0.2 mm clip over the left renal artery (2K1C) or a sham operation, some 2K1C rats were norm otensive. These rats and the sham rats then received an intravenous in fusion of AngII (4 ng/min) for 10 days. 4. AngII caused the 2K1C rats to attain significantly higher mean arterial pressure than the sham ra ts (152 +/- 7 vs 133 +/- 7 mmHg) and did not result in water or electr olyte retention in the 2K1C rats. 5. These results indicate that normo tensive 2K1C rats exhibit enhanced responsiveness to the slow presser effect of AngII and that the arterial pressure response to renal ischa emia may depend on both AngII formation and responsiveness to the chro nic actions of the peptide.