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Abstract

In a previous communication (Am J Hypert, 13 (4, part 2): 273A, 2000) we have reported that the experimental acute renal hypertension (EARH) which follows the reopening (REOP) of the right renal hilum after a period of complete renal ischaemia (functional right nephrectomy: FRN) was present only in rats nephrectomized on the controlateral side. The present report modifies our previous conclusion showing that the EARH is also present in rats with the controlateral left kidney intact. Blood pressure (BP), heart rate (HR), rate of breathing (RB), rectal temperature (T), urine flow rate, osmolality and Na+, K+ excretion from the right kidney were continuously monitored for one hour before, during FRN, and for one hour after REOP in pentobarbital anaesthetized, spontaneously breathing Sprague- Dawley (250-300g) rats with the left kidney intact (group 1) and in rats nephrectomized on the left side (group 2). In group 1 the REOP after a FRN of 30 (group 1a, n=5), 60 (group 1b, n=5), 180 (group 1c, n=5) min was followed by an average peak increase of 12.4 ± 2.7, 3.5 ± 1.2 and 47.5 ± 4.4 mmHg (mean ± S.E.) in systolic BP (SBP) respectively, and it was highly reproducible for FRN of 180 min only. In group 2 the REOP of the only remaining and completely ischaemic right kidney after 30 (group 2a, n=5), 60 (group 2b, n=5) and 180 (group 2c, n=5) min of FRN was followed by an average peak increase of 19.4 ± 4.3, 36.1 ± 11.0 and 72.8 ± 10.5 mmHg in SBP respectively. A marked tachycardia was observed in group 2c only. The i.v. injection of 3 mg/Kg of Irbesartan 30 min before REOP in 3 additional rats of group 2b, completely prevented the acute increase of BP observed in this group of rats. Plasma renin activity (PRA) measured 1 hour after REOP, was directly related to the duration of FRN, being maximal in group 1c and 2c, 63.9 ± 5 .9 and 57.5 ± 7.7 ng AI/ml/hr respectively. These data indicate that the EARH which follows the REOP of a completely ischaemic kidney is present either in rats with the controlateral kidney intact and in rats previously nephrectomized on the left side. Together with the effects of Captopril, the response to Irbesartan indicates that EARH is due to an acute release of renin and conseguent formation of angiotensin II, and thus it represents an useful experimental model of an acute angiotensin-mediated renal hypertension (J. Hypert 18:1277, 2000).

Acute renin release, Renal ischaemia, Functional right nephrectomy
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© American Journal of Hypertension, Ltd. 2001
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