Tohoku J. Exp. Med., 1999, 188 (4)

Renal Nerve Stimulation Induces a2-Adrenoceptor-Mediated Antinatriuresis under Inhibition of Prostaglandin Synthesis in Anesthetized Dogs

YOSHIHARU HAYASHI, KIYOSHI CHIBA, TOSHIYUKI MATSUOKA, MIZUE SUZUKI-KUSABA, MAKOTO YOSHIDA, HIROAKI HISA and SUSUMU SATOH

Laboratory of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578

  • The interaction between prostaglandins and a-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 mg•kg-1•min-1 ), an a1-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 mg•kg-1•min-1 ), an a2-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 a1- and a2-adrenoceptors mediate the RNS-induced antinatriuresis, but the a2-adrenoceptor-mediated portion is impaired by prostaglandins.
    Key words--- sympathetic nervous system; kidney; Na+ reabsorption; prazosin; yohimbine; indomethacin
    © 1999 Tohoku University Medical Press

    Tohoku J. Exp. Med., 1999, 188, 335-346
    Address for reprints: Hiroaki Hisa, Ph.D., Laboratory of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai 980-8578, Japan.
    e-mail: hhisa@mail.pharm.tohoku.ac.jp

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