Pressure natriuresis following acute and chronic inhibition of
nitric oxide synthase in rats.
Guarasci, Gregory R., and Robert L. Kline.
Department of Physiology, University of Western Ontario, London,
Ontario N6A 5C1, Canada
APStracts 2:0234R, 1995.
Pressure natriuresis following acute and chronic inhibition of nitric
oxide synthase in rats. Am. J. Physiol. --- Nitric oxide has been
suggested to be an essential mediator of pressure natriuresis. To
investigate this hypothesis, the effect of acute or chronic
inhibition of nitric oxide synthase on pressure natriuresis and renal
interstitial hydrostatic pressure was studied in anesthetized
Sprague-Dawley rats with fixed neural and hormonal influences on the
kidney. Both acute infusion (10 [mu]g x kg-1 x min-1, i.v.) and
chronic administration (50 mg x kg-1 x day-1 for 7 days in drinking
water) of NG-nitro-L-arginine methyl ester (L-NAME) resulted in
significantly increased mean arterial pressure, a 30% decrease in
renal blood flow, and no change in glomerular filtration rate when
compared with values in control rats. Pressure-diuresis, pressure
-natriuresis, and pressure-fractional sodium excretion curves in L
-NAME-treated rats were shifted to a higher pressure (by about 25 mm
Hg) when compared with those in control rats. The relationship
between renal artery pressure and renal interstitial hydrostatic
pressure was shifted similarly in L-NAME-treated rats. Acute
administration of L-arginine completely reversed the renal effects of
chronic L-NAME. These data indicate that at the doses used in this
study, both acute and chronic inhibition of nitric oxide synthase
decreased the ability of the kidney to excrete sodium at least in
part by a hemodynamic mechanism leading to an increased filtration
fraction and a decreased renal interstitial pressure. The parallel
shift of the pressure-natriuresis curve to a higher pressure suggests
that nitric oxide is an important modulator, but not an essential
mediator of the pressure natriuresis.
Received 23 March 1995; accepted in final form 15 August 1995.
APS Manuscript Number R194-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 August 1995.