Abrahams Z, Sutter M C
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Eur J Pharmacol. 1994 Feb 3;252(2):195-203. doi: 10.1016/0014-2999(94)90597-5.
The aim of this study was to determine if the stimulatory action of human gamma globulin on the spontaneous activity of the rat mesenteric portal vein is due to decreased K+ conductance. Glibenclamide potentiated the action of human gamma-globulin on the portal vein by 45% and on its own had a concentration- and time-dependent biphasic (increase followed by a decrease) effect on the spontaneous activity of the portal vein. Diazoxide and pinacidil both inhibited the action of human gamma-globulin on the rat mesenteric portal vein. Levcromakalim (BRL 38227) potentiated the stimulatory action of human gamma-globulin on the integrated force of the spontaneous contractions of the rat mesenteric portal vein by 40% and 49% at concentrations of 0.5 and 5 microM, respectively. These studies suggest that human gamma-globulin can act by directly modulating a K+ channel.
本研究的目的是确定人γ球蛋白对大鼠肠系膜门静脉自发活动的刺激作用是否归因于钾离子电导降低。格列本脲使γ球蛋白对门静脉的作用增强了45%,其自身对门静脉自发活动有浓度和时间依赖性的双相(先增加后降低)效应。二氮嗪和平尼地尔均抑制人γ球蛋白对大鼠肠系膜门静脉的作用。分别在浓度为0.5和5微摩尔时,左旋克罗卡林(BRL 38227)使γ球蛋白对大鼠肠系膜门静脉自发收缩综合力的刺激作用增强了40%和49%。这些研究表明,人γ球蛋白可通过直接调节钾离子通道发挥作用。