Nitric oxide regulates hco3- and na+ transport by a cgmp mediated
mechanism in the kidney proximal tubule.
Wan, Tong.
Department of Cellular and Molecular Physiology, Yale University
School of Medicine, New Haven, CT 06520
APStracts 3:0200F, 1996.
The effects of nitric oxide (NO) on blood pressure and renal
hemodynamics are well established but those of NO on renal tubule
bicarbonate (HCO3- ) and Na+ transport are not fully understood. In
this study we combined renal clearance and in situ microperfusion
techniques to investigate the effects of NO on the renal excretion of
Na (FENa%) and the rates of renal tubule absorption of fluid (JV )
and bicarbonate (JHCO3) in the rat kidney. Administration of the
nitric oxide synthase inhibitor L-NAME (NG-nitro-L-arginine methyl
ester), 6mg/kg by bolus iv, did not change mean blood pressure and
GFR significantly. However, L-NAME significantly increased urine flow
rate and FENa%, and these effects were maintained over a 60 minute
period. Addition of L-NAME markedly decreased both Jv and JHCO3 in
the proximal tubule. In contrast, addition of 1[mu]M sodium
nitroprusside (SNP) or S-nitroso-N-acetylpenicillamine (SNAP),
significantly increased both JV and JHCO3. Similar stimulation was
also observed when 8-Br cGMP (1[mu]M) was added to the luminal
perfusate. The stimulatory effects of SNP and 8-Br cGMP on Jv and
JHCO3 were not additive. The increments in Jv and JHCO3 due to SNP
were abolished by the Na+/H+-exchange blocker EIPA and the guanylate
cyclase inhibitor methylene blue. These results indicate that NO
stimulates proximal tubule Na+ and HCO3- transport through a cGMP
-linked pathway in the kidney proximal tubule.
Received 8 March 1996; accepted in final form 24 October 1996.
APS Manuscript Number F81-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996