Renal nerve stimulation induces _γ2-adrenoceptor-mediated antinatriuresis under inhibition of prostaglandin synthesis in anesthetized dogs

The interaction between prostaglandins and α-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 μg • kg^-1 • min^-1), an α₁-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 μg • kg^-1 • min^-1), an α₂-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 α₁ and α₂-adrenoceptors mediate the RNS-induced antinatriuresis, but the α₂-adrenoceptor-mediated portion is impaired by prostaglandins. - sympathetic nervous system; kidney; Na⁺ reabsorption; prazosin; yohimbine; indomethacin