Endogenous angiotensin ii chronically supports renal and lumbar
sympathetic nerve activity in sodium-deprived, conscious rats.
Xu, Ling, and Virginia L. Brooks.
Department of Physiology and Pharmacology, The Oregon Health
Sciences University, Portland, OR 97201-3098, (503) 494-5843, FAX:
(503) 494-4352
APStracts 3:0299H, 1996.
The hypothesis that chronic elevations in endogenous angiotensin II
(AII) increase sympathetic outflow in conscious, normotensive rats
was tested by determining if acute blockade of AII receptors with
losartan (10 mg/kg, iv) decreases renal (RSNA) or lumbar sympathetic
nerve activity (LSNA) or heart rate (HR) more in rats with higher AII
levels due to a low sodium diet (LS) compared to a control sodium
(CS) or high sodium (HS) diet. In LS rats, losartan decreased
(p<0.05) MAP in two phases: an immediate decrease of 23+/-2 mmHg
and a slower fall to 35+/-4 mmHg below control 40 min post-losartan.
Five min after losartan, RSNA (149+/-13%), LSNA (143+/-5%) and HR
(109+/-2%) were increased (p<0.05). Despite further falls in
MAP, the elevation in RSNA and HR remained constant and LSNA
decreased toward control (119+/-4%). Following restoration of MAP to
basal levels with methoxamine or phenylephrine infusion, RSNA (46+/
-8%), LSNA (49+/-11%) and HR (76+/-2%) were suppressed (p<0.05).
In CS rats, losartan also initially decreased (p<0.05) MAP by
6+/-2 mmHg and increased (p<0.05) RSNA to 129+/-13%. When MAP
was returned to control, RSNA was decreased (70+/-8%; p<0.05),
but less than in LS rats. In contrast, no changes in MAP, RSNA, LSNA
or HR were observed after losartan in HS rats. In conclusion,
endogenous AII chronically supports RSNA, LSNA and HR in conscious,
normotensive low and normal sodium intake rats.
Received 26 March 1996; accepted in final form 1 July 1996.
APS Manuscript Number H287-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996