摘要
外周型苯二氮受体的配体PK11195增强大鼠肾上腺皮质球状带细胞醛固酮分泌的效应可被主要作用于胞浆膜Ca^(2+)通道的阻断剂硝苯啶所取消,而不被选择性作用于线粒体Ca^(2+)通道的阻断剂硝苯啶呋海因(Da—ntrolene)所取消。PK11195在其增强醛固酮分泌的最大效应条件下并不影响球状带细胞内cAMP水平。本文的结果表明苯二氮(?)受体调控醛固酮分泌的机制中,细胞内信使物质不是cAMP,也不是来自线粒体的Ca^(2+),而是来自胞浆膜外的Ca^(2+)。
PR11195, a ligand of peripheral-type benzodiazepine receptor can stimulate the aldosterone secretion of isolated adrenal glomerulosa cells;this effect could be abolished by nifedipine which mainly blocks the calcium channel in plasma membrane, but could not be abolished by dantrolene, a selective blocker of mitochondria calcium channel. Even under the conditions of the maximum stimulative effects on aldosterone secretion, PK11195 could not change the cyclic AMP(cAMP)content in isolated glomerulosa cells. These results indicated that in the modulatary mechanism of benzodiazepine receptor on aldosterone secretion, the intracellular messenger might be the Ca from extracellular Ca pool, but not the Ca from mitohondrial Ca pool or cAMP.
出处
《第一军医大学学报》
CSCD
1989年第2期94-97,共4页
Journal of First Military Medical University
关键词
醛固酮
苯二氮zhao
钙离子
CAMP
adrenal glomerulosa cell
aldosterone
benzodiazepine receptor
calcium ion
cyclic AMP.
