Role of calcium and sodium ions in the inhibitory control of baseline and stimulated prolactin release.
The mechanism of dopamine (DA) inhibition of pituitary PRL release is still unclear. To study it, we utilized enzymatically dispersed anterior pituitary cells obtained from adult female Sprague-Dawley rats. The cells were incubated in media with or without Na+ and in the presence or the absence of various drugs for 30 min for evaluating the secretion of PRL under baseline and experimental conditions. In some experiments, 45Ca2+ (1 microCi/ml) was added after 30 min of incubation and the latter prolonged for an additional minute to determine Ca2+ uptake. DA inhibited baseline PRL release and 45Ca2+ uptake in a dose-dependent manner only in the presence of Na+ and was totally inactive in its absence. The inhibitory effects of Nifedipine and Nicardipine, two Ca2+ channel antagonists, on PRL release were also found to be Na+ dependent. BAY K 8644, a Ca2+ channel agonist, stimulated PRL release and Ca2+ uptake in a dose-dependent manner, and these effects were enhanced by Na+-free media. DA antagonized the stimulatory actions of BAY K 8644 on PRL release in a similar dose-dependent manner both in the presence and the absence of Na+. However, on stimulated 45Ca2+ uptake DA was less effective in the absence of Na+. The stimulatory action of TRH on PRL release was enhanced by the absence of Na+. DA antagonized the effect of TRH in a dose-dependent manner both in the presence and in the absence of Na+ but appeared more effective in the absence of the ion. The PRL-releasing effects of phorbol ester and of the Ca2+ ionophore A23187 were antagonized by DA in a Na+- independent manner. These results suggest the existence of two mechanisms of DA inhibitory action: one exerted on baseline PRL release which is Na+ dependent, receptor linked, and probably implicates potential operated Ca2+ channels; the other is exerted on stimulated PRL release, is Na+ independent, and appears to be a postreceptorial intracellular event probably involving protein kinase C and/or cytosolic Ca2+ levels.
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D004298:Dopamine / Q000494:pharmacology; D005260:Female; D009529:Nicardipine / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D010703:Phorbol Esters / Q000494:pharmacology; D011388:Prolactin / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000502:physiology*; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology
D010703:Phorbol Esters; D000001:Calcimycin; D013973:Thyrotropin-Releasing Hormone; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D011388:Prolactin; D012964:Sodium; D009529:Nicardipine; D009543:Nifedipine; D002118:Calcium; D004298:Dopamine