Relationship between basal no release and cyclooxygenase products
in the normal rat kidney.
Baylis, Chris, Brigitte Slangen, Sarah Hussain, and Carol Weaver.
Department of Physiology, Medicine and Physical Therapy, West
Virginia University, Morgantown, WV 26506-9229 and Department of
Obstetrics and Gynecology, Academisch Ziekenhuis Maastricht, Postbus
5800, 6202AZ, MAASTRICHT, Netherlands
APStracts 3:0278R, 1996.
We investigated the physiologic regulation of renal function by nitric
oxide (NO) and its interactions with the endothelial cyclooxygenase
products, in the conscious chronically catheterized rat. A subpressor
dose of NO inhibitor nitro-L-arginine methyl ester (L-NAME), produced
renal vasoconstriction that was unaffected by cyclooxygenase
inhibition with indomethacin (INDO). Acute, high dose L-NAME produced
a pressor response of 40mm Hg and marked renal vasoconstriction. INDO
selectively amplified the renal vasoconstriction, whereas inhibition
of the thromboxane/endoperoxide receptor, had no effect. Chronic NO
inhibition for 5 weeks led to sustained hypertension and renal
vasoconstriction, the latter was amplified by acute INDO. These data
suggest that in the normal, conscious rat the kidney is under
important NO-dependent tone. There is no obvious interaction between
NO and the cyclooxygenase products in control of basal renal
function. When systemic NO inhibition is produced with either acute
or chronic high dose L-NAME, the kidney is severely vasoconstricted.
The renal vasoconstriction is not ameliorated by
thromboxane/endoperoxide antagonism but is exacerbated by
cyclooxygenase blockade, suggesting that vasodilator cyclooxygenase
products compensate for the renal hypoperfusion due to severe NO
deficiency.
Received 16 May 1995; accepted in final form 6 May 1996.
APS Manuscript Number R297-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996