Calcium channel and prolactin release in rat clonal pituitary cells: effects of verapamil.
Effects of verapamil on membrane electrical properties and prolactin release were studied in a rat anterior pituitary cell line GH3. Thyrotropin-releasing hormone (TRH), Ba2+, and high concentration of K+ enhance the release of prolactin from GH3 cells. These stimulatory actions on prolactin release were inhibited by adding 10(-4) M verapamil to the bathing mediums. The maximum rate of rise of the Ca action potential was reduced to 17% of the control by addition of 10(-4) M verapamil. Ba2+ caused a sustained membrane depolarization because Ba2+ goes through the Ca channels and blocks the development of the delayed rectification. This effect of Ba2+ was also inhibited by verapamil. Verapamil suppressed both the Na+ and outward K+ currents in addition to the Ca2+ current. The suppressive effect of verapamil on the voltage-sensitive Ca current is probably responsible for the inhibition of TRH- and high K+-stimulated prolactin release because the suppression of the Na+ and outward K+ currents does not inhibit the stimulatory actions of these secretagogues.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D010911:Pituitary Neoplasms / Q000378:metabolism* / Q000503:physiopathology; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology*
D007473:Ion Channels; D013779:Tetrodotoxin; D011388:Prolactin; D012964:Sodium; D014700:Verapamil; D002118:Calcium