Changes in plasma ACE activity during the development and reversal of one-kidney, one clip hypertension in rats

Plasma angiotensin converting enzyme (ACE) activity was studied during the development and the reversal of one-kidney, one clip (1K1C) renal hypertension in rats (RHR). Plasma ACE activity was measured in RHR 1 (n = 11), 3 (n = 8), 6 (n = 12), 14 (n = 7), and 80-120 days (n = 17) after clipping. Plasma ACE activity (nmol/min/ml) was elevated (p less than 0.05) in chronic RHR (80-120 days; mean arterial pressure, MAP: 216 +/- 9 mmHg), being 142 +/- 14 (n = 17) vs. 100 +/- 3.2 (n = 20) for normotensive control rats (MAP: 116 +/- 3 mmHg), whereas no significant differences were observed at earlier times. Overactivity of the renin-angiotensin system (RAS) was demonstrated indirectly by the reduction of MAP (greater than 15 mmHg) in response to captopril (10 mg/kg, i.v.) only during the first 3 days after clipping and in chronic severely hypertensive rats. In another experiment, ACE activity in chronic RHR was measured serially before and 1, 6 and 24 hours after unclipping. Serial measurements of plasma ACE showed a progressive decrease from 145 +/- 26 to 122 +/- 21, 24 hours after unclipping (n = 7, p less than 0.05, paired Student t-test) when MAP was reduced from 204 +/- 15 to 113 +/- 7 mmHg. There was essentially no change during 24 hours from the initial values of RHR-sham (MAP: 206 +/- 5 mmHg, ACE: 140 +/- 19, n = 8) and normal rats-sham (MAP: 115 +/- 2 mmHg, ACE: 96 +/- 3, n = 6). These data provide further evidence that chronic renal hypertension is associated with important changes in the metabolism of vasoactive peptides.