Effects of a reversible 'nephrectomy' on renal sympathetic activity and blood pressure in the rat: evidence for an acute angiotensin-mediated hypertension.
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.
Recordati
G
G
Istituto di Clinica Medica Generale e Terapia Medica, Centro di Fisiologia Clinica ed Ipertensione, Università di Milano, Italy. giorgio.recordati@unimi.it
Zorzoli
F
F
Zanchetti
A
A
D000208:Acute Disease; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000809:Angiotensins / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D006339:Heart Rate / Q000502:physiology; D006400:Hematocrit; D006977:Hypertension, Renal / Q000188:drug therapy / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply / Q000294:innervation* / Q000601:surgery; D008297:Male; D009392:Nephrectomy / Q000379:methods*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013564:Sympathetic Nervous System / Q000502:physiology*
D000806:Angiotensin-Converting Enzyme Inhibitors; D000809:Angiotensins; D002216:Captopril