Ozawa S, Kimura N
Am J Physiol. 1982 Jul;243(1):E68-73. doi: 10.1152/ajpendo.1982.243.1.E68.
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.
在大鼠垂体前叶细胞系GH3中研究了维拉帕米对膜电特性和催乳素释放的影响。促甲状腺激素释放激素（TRH）、Ba2+和高浓度K+可增强GH3细胞催乳素的释放。向浴液中加入10(-4)M维拉帕米可抑制这些对催乳素释放的刺激作用。加入10(-4)M维拉帕米后，Ca动作电位的最大上升速率降至对照的17%。Ba2+引起持续的膜去极化，因为Ba2+通过Ca通道并阻断延迟整流的发展。维拉帕米也抑制了Ba2+的这种作用。维拉帕米除了抑制Ca2+电流外，还抑制Na+和外向K+电流。维拉帕米对电压敏感性Ca电流的抑制作用可能是其抑制TRH和高K+刺激的催乳素释放的原因，因为对Na+和外向K+电流的抑制并不抑制这些促分泌剂的刺激作用。
