The effects of halothane on renal hemodynamics and the nitric oxide (NO)-gu
anylate cyclase signaling pathway were examined in anesthetized rabbits usi
ng a renal microdialysis method. Halothane (0.5 and 2 vol%) caused dose-dep
endent decreases in blood pressure, renal blood flow and the renal intersti
tial concentrations of guanosine 3',5'-cyclic monophosphate (cGMP) or nitra
te (NO2)/nitrite (NO3). Sodium nitroprusside (20 mu g kg(-1) min(-1), i.v.)
under the inhalation of halothane (2 vol%) increased the renal interstitia
l concentration of cGMP. L-Arginine (priming dose, 300 mg kg(-1) 10 min(-1)
; sustaining dose, 50 mg kg(-1) min(-1), i.v.) did not reverse halothane-in
duced reductions of cGMP and NO2/NO3. These findings demonstrate that halot
hane caused a renal vasoconstriction and inhibited the NO-guanylate cyclase
signaling pathway in the kidney. Moreover, it is possible that the renal h
emodynamic responses to halothane might have been induced, in part, through
this inhibition. Finally, it can be assumed that halothane did not interfe
re with the activation process of guanylate cyclase by NO. (C) 1999 Elsevie
r Science B.V. All rights reserved.