title: The loss of 45Ca2+ associated with prolactin release from the tilapia (Oreochromis mossambicus) rostral pars distalis.
abstract: The relationship between tritium 3H-labeled prolactin (PRL) release and the loss of tissue-associated 45Ca2+ was examined in the tilapia rostral pars distalis (RPD) using perifusion incubation under conditions which inhibit or stimulate PRL release. Depolarizing [K+] (56 mM) and hyposmotic medium (280 mOsmolal) increased both the release of [3H]PRL and the loss of 45Ca2+. The responses to high [K+] were faster and shorter in duration than those produced by reduced osmotic pressure. The depletion of Ca2+ from the incubation medium with 2 mM EGTA suppressed the [3H]PRL response evoked by high [K+] or reduced osmotic pressure. Exposing the tissues to Ca(2+)-depleted medium in the absence of high [K+] or reduced osmotic pressure produced a sharp, but brief, increase in 45Ca2+ loss. Cobalt (10(-3) M), a competitive inhibitor of calcium-mediated processes, inhibited the [3H]PRL response to hyposmotic medium and to high [K+]. Cobalt also diminished the increased loss of 45Ca2+ evoked by exposure to reduced osmotic pressure, but was ineffective in altering responses to high [K+]. Methoxyverapamil (D600; 10(-5) M), a blocker of certain voltage-sensitive Ca2+ channels, did not alter either the [3H]PRL or the 45Ca2+ responses to high [K+] and reduced osmotic pressure. Taken together with our earlier studies, the present findings suggest that exposure to high [K+] or hyposmotic medium produces rapid changes in the Ca2+ metabolism of the tilapia RPD that are linked to the stimulation of PRL secretion. Nevertheless, the increased 45Ca2+ loss, but not [3H]PRL release, upon exposure to Ca(2+)-depleted media suggests that Ca2+ loss may not always reflect intracellular events that lead to PRL release.
authors.affiliation: Department of Zoology, University of Hawaii, Honolulu 96822.
authors.forename: N H
authors.initials: NH
authors.lastname: Richman
authors.forename: C A
authors.initials: CA
authors.lastname: Ford
authors.forename: L M
authors.initials: LM
authors.lastname: Helms
authors.forename: I M
authors.initials: IM
authors.lastname: Cooke
authors.forename: P K
authors.initials: PK
authors.lastname: Pang
authors.forename: E G
authors.initials: EG
authors.lastname: Grau
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003035:Cobalt / Q000378:metabolism; D005260:Female; D005711:Gallopamil / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009997:Osmotic Pressure; D010473:Perciformes / Q000378:metabolism*; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism*
chemical_list: D005711:Gallopamil; D003035:Cobalt; D011388:Prolactin; D011188:Potassium; D002118:Calcium