Factors influencing acute ischaemia-induced renal hypertension in rats.

Abstract

To verify if the acute hypertension that occurs after reversal of complete renal ischaemia is related to the duration of ischaemia, is different in one-kidney (1K) and two-kidney (2K) rats, and is prevented by angiotensin receptor blockade. Four groups of Sprague-Dawley rats anaesthetized with pentobarbitone were studied before, during and after a reversible, complete renal ischaemia achieved by functional right nephrectomy. In 1K rats (group 1, n = 21), reopening of right renal hilum after functional right nephrectomy of 180, 60 and 30 min was followed by peak increases in systolic blood pressure of 76.0 10.1 mmHg, 36.5 10.0 mmHg and 18.4 4.4 mmHg, respectively (mean SEM). In 2K rats (group 2, n = 21), functional right nephrectomy of 180, 60 and 30 min was followed by smaller increases in blood pressure of 49.8 7.6 mmHg, 5.9 3.3 mmHg and 8.3 2.1 mmHg, respectively. Plasma renin activity was directly related to the duration of functional right nephrectomy, and was greater in 1K rats. In group 3, irbesartan administered to 1K rats (n = 8) during functional right nephrectomy almost completely prevented the development of hypertension upon reopening. In group 4, labetalol injected intravenously in 1K rats (n = 3) did not prevent the blood pressure surge at reopening (49.2 8.5 mmHg). An experimental acute renal hypertension may be elicited both in 1K and in 2K rats and for functional right nephrectomy of 30, 60 and 180 min duration. The increase in blood pressure is proportional to the duration of functional right nephrectomy and greater in 1K than in 2K rats. The experimental acute renal hypertension is due to acute release of renin and generation of endogenous angiotensin II, and is specifically prevented by the angiotensin II type 1 receptor blocker, irbesartan, but not by labetalol.