EVIDENCE THAT CA2+-ACTIVATED K+ CHANNELS PARTICIPATE IN THE REGULATION OF PITUITARY PROLACTIN SECRETION

We evaluated the role of Ca2+-activated K+ channels in the regulation of prolactin (PRL) secretion with a perifusion system using acutely dispersed rat anterior pituitary cells. Apamin, which blocks Ca2+-activated K+ channels, induced PRL secretion in a dose-dependent fashion between 1 and 300 nM (r = 0.99, P < 0.01). Charybdotoxin, another Ca2+-activated K+ channel-blocker, also induced PRL secretion at 20 nM concentration. These were not non-specific toxic effects, since stimulation of PRL secretion by 10 nM thyrotropin-releasing hormone (TRH) was not different before and after applying the channel-blockers. Both 10 mu M dopamine and 2 mu M nifedipine significantly, but incompletely, depressed PRL secretion induced by 100 nM apamin; 10 mu M dopamine completely blocked PRL secretion induced by 20 nM charybdotoxin. Our data indicate that Ca2+-activated K+ channels may play an important role in the regulation of PRL secretion.