Modulation by leu-enkephalin of peptide release from perifused neurointermediate pituitary. I. Selective effect on potassium-, veratridine- and isoproterenol-stimulated secretion of vasopressin.
This study examines the effect of leu-enkephalin on K+, veratridine and isoproterenol stimulation of vasopressin (AVP) release from perifused neurointermediate pituitaries of rats. As opposed to catecholamine-evoked release of peptide, the secretory response to high K+ and veratridine involves Ca2+ influx, as the effect of both factors was blocked by Ca-chelation and the channel blocker D 600. Leu-enkephalin was found to antagonize AVP secretion induced by K+ and veratridine depolarization, by acting through a naloxone-sensitive receptor system. In contrast, the opiate failed to significantly affect isoproterenol-stimulated release of AVP, which we show to be correlated to cAMP accumulation in pure neurohypophyseal tissue. These results support the view that opiates modulate AVP secretion triggered by depolarization of nerve terminals by regulating Ca2+ fluxes.
D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004743:Enkephalin, Leucine / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D010904:Pituitary Gland, Posterior / Q000187:drug effects*; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D014701:Veratridine / Q000494:pharmacology*; D014702:Veratrine / Q000031:analogs & derivatives*
D007473:Ion Channels; D001127:Arginine Vasopressin; D004743:Enkephalin, Leucine; D014701:Veratridine; D014702:Veratrine; D007545:Isoproterenol; D011188:Potassium; D002118:Calcium