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1 Departamento de Fisiología, Facultad de Medicina, 30100-Murcia, Spain; and 2 Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
The present study evaluated whether
inhibition of guanylyl cyclase (GC) with
1H-(1,2,4)oxadiazolo[4,3-a]quinoxaline-1-one (ODQ) and
methylene blue (MB) or inhibition of the renal metabolism of
arachidonic acid by cytochrome P-450 (CYP450) enzymes with 1-aminobenzotriazole (ABT) and N-hydroxy-N'-(4
butyl-2-methyl phenyl)formamidine (HET0016) alters the renal tubular
and vascular effects of a nitric oxide (NO) donor in vivo. Intrarenal
infusion of ODQ or MB at a dose of 170 nmol · kg
1 · min1 lowered
renal blood flow (RBF) by 30 and 15%, respectively; glomerular filtration rate (GFR) by 26 and 18%, respectively; and sodium and
water excretion by ~35%. In rats pretreated with
nitro-L-arginine methyl ester (37 nmol · kg1 · min1) to block
the endogenous production of NO, intrarenal infusion of the NO donor
S-nitroso-N-acetylcysteine (S-NO-NAC; 50 nmol · kg1 · min1) increased
RBF (18%), sodium (73%), and water excretion (61%). ODQ or MB
administration blocked the effect of S-NO-NAC on RBF but not the
diuretic and natriuretic response. Pretreatment of rats with ABT or
HET0016 also abolished the renal vasodilatory response to the NO donor
and reduced its diuretic and natriuretic effect. These results indicate
that both activation of GC and inhibition of CYP450 enzymes contribute
to the renal vascular actions of NO, whereas the natriuretic and
diuretic actions of NO appear to be largely CYP450 dependent.
renal hemodynamics; kidney; guanosine 3',5'-cyclic monophosphate; 20-hydroxytetraenoic acid; epoxyeicosatrienoic acids
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