Abstract
The aim of the present study was to characterize the acute hypertensive and tachycardic episode which follows the reopening (REOP) of the right kidney hylus after a period of complete renal ischemia produced by discrete ligatures of the renal artery and vein (functional right nephrectomy: FRN). 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 1–3 hours after REOP in pentobarbital anesthetized, 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 REOP after a FRN of 30 and 60 min was followed by only slight and insignificant changes in BP and HR. In group 2 the REOP of the only remaining and completely ischemic right kidney after 30 (group 2a, n = 5), 60 (group 2b, n = 3) and 180 (group 2c, n = 5) min of FRN was followed by an average peak increase of 23.0 ± 4.3, 49.1 ± 14.1 and 72.8 ± 10.5 mmHg in systolic BP respectively. A marked tachycardia was observed in group 2c only. In an additional group of left nephrectomized rats a i.v. bolus injection of 3 mg/Kg Captopril 15 and 30 min before REOP (n = 5), almost completely prevented the development of hypertension and tachycardia. In two animals i.v. Captopril injections at the peak of the hypertensive episode quickly returned BP to normal. These data indicate that in mononephrectomized rats (group 2) the hypertension (and tachycardia) which follows the REOP of the completely ischemic and only remaining kidney is due to acute release of renin and the consequent generation of angiotensin II. These effects are absent if the left kidney is intact (group 1). This finding points to an interaction between an intact kidney and renin release from an ischemic kidney or the peripheral response to angiotensin II. Our observations also offer an experimental model of an acute angiotensin II-mediated hypertensive response of renal origin.
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