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.