Renal nerve stimulation induces alpha2-adrenoceptor-mediated antinatriuresis under inhibition of prostaglandin synthesis in anesthetized dogs.
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.
Hayashi
Y
Y
Laboratory of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.
Chiba
K
K
Matsuoka
T
T
Suzuki-Kusaba
M
M
Yoshida
M
M
Hisa
H
H
Satoh
S
S
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000758:Anesthesia; D000818:Animals; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000294:innervation* / Q000502:physiology; D008297:Male; D009318:Natriuresis / Q000187:drug effects / Q000502:physiology*; D011224:Prazosin / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D011453:Prostaglandins / Q000096:biosynthesis*; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology*; D012964:Sodium / Q000378:metabolism; D015016:Yohimbine / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D016861:Cyclooxygenase Inhibitors; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D018341:Receptors, Adrenergic, alpha-2; D015016:Yohimbine; D012964:Sodium; D011224:Prazosin; D007213:Indomethacin