Flunarizine, a calcium influx blocker, inhibits TRH-but not potassium-stimulated prolactin secretion.
The effect of flunarizine on the secretion of prolactin from monolayer cultures of normal rat pituitary cells has been determined. Both basal and TRH-stimulated secretion were found to be significantly inhibited by micromolar concentrations of flunarizine, whereas depolarization (high K+)-stimulated secretion was virtually unaffected. These results indicate that TRH-stimulated prolactin secretion probably involves calcium influx and that flunarizine may be useful as a probe for particular Ca2+ channels.
D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002478:Cells, Cultured; D002936:Cinnarizine / Q000031:analogs & derivatives / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005444:Flunarizine; D008297:Male; D010879:Piperazines / Q000494:pharmacology*; D010903:Pituitary Gland, Anterior / Q000187:drug effects* / Q000378:metabolism; D011188:Potassium / Q000494:pharmacology*; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013973:Thyrotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000494:pharmacology*
D002121:Calcium Channel Blockers; D010879:Piperazines; D002936:Cinnarizine; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D005444:Flunarizine; D011188:Potassium