AUGMENTATION OF ANGIOTENSIN-II RELEASE FROM ISOLATED MESENTERIC-ARTERIES OF WISTAR-KYOTO AND SPONTANEOUSLY HYPERTENSIVE RATS FOLLOWING NEPHRECTOMY

1. We previously reported that angiotensin II release from the mesente ric arteries of Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) increased in a time-dependent manner as a result of the isolati on of the arteries and perfusion. This phenomenon appeared to be due t o the withdrawal of circulating angiotensin II (AII). 2. The purpose o f the present study was to test the hypothesis that vascular AII gener ation may be negatively regulated by circulating AII in WKY and SHR, a nd to clarify the role of this vascular angiotensin II in the sustaine d hypertension of SHR following nephrectomy. 3. The mesenteric arterie s from kidney-intact and nephrectomized WKY and SHR were perfused and the amount of AII released into the perfusate was measured. The effect s of the angiotensin converting enzyme inhibitor, captopril, and the e ffects of supplementation of renal renin and circulating angiotensins to nephrectomized rats, by blood exchange between kidney-intact and ne phrectomized rats, on AII release were examined to clarify the pathway of vascular AII generation after nephrectomy. 4. Nephrectomy caused a ugmentation of vascular AII release both in WKY and SHR in spite of th e abolishment of circulating renin. Captopril reduced this enhanced re lease of AII, but blood exchange did not affect it. There was no signi ficant difference in these responses between WKY and SHR. 5. These res ults suggest that WKY and SHR have in common a potent pathway for prod uction of vascular AII in response to the withdrawal of circulating AI I, although this pathway is not responsible for the sustained hyperten sion of SHR after nephrectomy. The precise pathophysiological role of this pathway remains to be elucidated.