Effects of a reversible 'nephrectomy' on renal sympathetic activity and blood pressure in the rat: evidence for an acute angiotensin-mediated hypertension
Recordati, G.; Zorzoli, F.; Zanchetti, A.
Journal of Hypertension 18(9): 1277-1287
2000
ISSN/ISBN: 0263-6352 PMID: 10994759 Document Number: 515360
Objective: To verify whether the normal kidney exerts a supportive, facilitatory action on renal sympathetic nerve activity (RSNA), the effects of unilateral and bilateral nephrectomy on RSNA have been studied. Methods: The RSNA, rectal temperature (T), rate of breathing (RB), arterial blood pressure (BP) and heart rate (HR) were continuously recorded in three groups of pentobarbital anaesthetized, spontaneously breathing Sprague-Dawley rats: group 1 (n = 5): both kidneys intact; group 2 (n = 5): left surgical nephrectomy; group 3 (n = 5): left surgical nephrectomy and functional exclusion of the right kidney (functional right nephrectomy, FRN), produced by a tight ligature of the renal hilum which was maintained for 3 h. In a fourth group (n = 7), in which nerve activity was not recorded, reopening of the right renal hilum was preceded or followed by intravenous administration of captopril (3 mg/kg). Results: In groups 1 and 2 RSNA increased from 22.3 +- 2.1 to 122.9 +- 13.6 and from 26.7 +- 1.2 to 93.2 +- 14.0 impulses/s (mean +- SEM), respectively, without concomitant changes in cardiovascular parameters. In group 3 RSNA decreased from 39.1 +- 3.1 to 13.7 +- 2.6 impulses/s during the 3 h of FRN. In group 3 the reopening of the right renal hilum was followed by a marked increase in BP and HR that was prevented or reversed by intravenous captopril in rats of group 4. Conclusions: The decrease in RSNA observed in rats during bilateral nephrectomy, in contrast to the increase observed in rats with one or both kidneys intact, suggests that the kidney as a whole exerts a supportive role on sympathetic nerve activity. The hypertension and tachycardia that follows the reopening of the right kidney hilum appears to be caused by the generation of endogenous angiotensin II; this is the first evidence of an acute angiotensin-mediated renal hypertension.