Effects of halothane on renal hemodynamics and interstitial nitric oxide in rabbits

The effects of halothane on renal hemodynamics and the nitric oxide (NO)-guanylate cyclase signaling pathway were examined in anesthetized rabbits using a renal microdialysis method. Halothane (0.5 and 2 vol%) caused dose-dependent decreases in blood pressure, renal blood flow and the renal interstitial concentrations of guanosine 3',5'-cyclic monophosphate (cGMP) or nitrate (NO2)/nitrite (NO3). Sodium nitroprusside (20 microg kg(-1) min(-1), i.v.) under the inhalation of halothane (2 vol%) increased the renal interstitial 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-induced reductions of cGMP and NO2/NO3. These findings demonstrate that halothane caused a renal vasoconstriction and inhibited the NO-guanylate cyclase signaling pathway in the kidney. Moreover, it is possible that the renal hemodynamic responses to halothane might have been induced, in part, through this inhibition. Finally, it can be assumed that halothane did not interfere with the activation process of guanylate cyclase by NO.