Renal Nerve Stimulation Induces .ALPHA.2-Adrenoceptor-Mediated Antinatriuresis under Inhibition of Prostaglandin Synthesis in Anesthetized Dogs.

Abstract

The interaction between prostaglandins and alpha-adrenoceptors in neural control of tubular sodium reabsorption was examined in anesthetized dogs. Renal nerve stimulation (RNS; 0.5-1.0 Hz, 10 V, 1.0-milliseconds duration) reduced fractional excretion of Na+ (FENa) with minimal changes in hemodynamics and glomerular filtration. Intrarenal arterial infusion of prazosin (0.7 microg x kg(-1) x min(-1)), an alpha1-adrenoceptor antagonist, inhibited the RNS-induced reduction in FENa. However, the RNS-induced reduction in FENa was resistant to prazosin under pretreatment with indomethacin (5 mg/kg, i.v.), a cyclooxygenase inhibitor. Intrarenal arterial infusion of yohimbine (1 microg x kg(-1) x min(-1)), an alpha2-adrenoceptor antagonist, failed to inhibit the RNS-induced reduction in FENa in the absence or presence of indomethacin, but combined infusion of prazosin and yohimbine abolished the RNS-induced reduction in FENa in the presence of indomethacin. These results suggest that both alpha1- and alpha2-adrenoceptors mediate the RNS-induced antinatriuresis, but the alpha2-adrenoceptor-mediated portion is impaired by prostaglandins.