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

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Abstract
1. We have shown previously that renal artery stenosis in rats causes enhanced responsiveness to the slow pressor 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 degree of renal artery stenosis that was insufficient to raise blood pressure was able to enhance responsiveness to the slow pressor 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 normotensive. These rats and the sham rats then received an intravenous infusion of AngII (4 ng/min) for 10 days. 4. AngII caused the 2K1C rats to attain significantly higher mean arterial pressure than the sham rats (152 +/- 7 vs 133 +/- 7 mmHg) and did not result in water or electrolyte retention in the 2K1C rats. 5. These results indicate that normotensive 2K1C rats exhibit enhanced responsiveness to the slow pressor effect of AngII and that the arterial pressure response to renal ischaemia may depend on both AngII formation and responsiveness to the chronic actions of the peptide.