Renal nerve stimulation induces γ2-adrenoceptor-mediated antinatriuresis under inhibition of prostaglandin synthesis in anesthetized dogs

Yoshiharu Hayashi, Kiyoshi Chiba, Toshiyuki Matsuoka, Mizue Suzuki-Kusaba, Makoto Yoshida, Hiroaki Hisa, Susumu Satoh

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3 Citations (Scopus)


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

Original languageEnglish
Pages (from-to)335-346
Number of pages12
JournalTohoku Journal of Experimental Medicine
Issue number4
Publication statusPublished - 1999 Aug

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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