摘要
为研究糖皮质激素对原代培养大鼠肾上腺嗜铬细胞（AMCC）受激动所致儿茶酚胺的快速作用，用HPLC－ED方法检测了乙酰胆碱（10－5mol／L）、烟碱（10－5mol／L）、毒蕈碱（10－5mol／L）及55mmol／L的KCl在20min内所引起的儿茶酚胺量．地塞米松（Dex，10－4mol／L及10－5mol／L）及皮质酮（10－5mol／L）可以抑制AMCC的儿茶酚胺分泌；10－7mol／L的17β-雌二醇不能抑制，但10－5mol／L的可以抑制其分泌；醛固酮、雄烯二酮及胆固醇无抑制效应。为了揭示与分泌有关的细胞内变化，用SPex检测系统检测了细胞内钙（［Ca2+］）的含量。发现地塞米松及皮质酮有抑制因乙酰胆碱、烟碱、毒蕈碱及高K+所引起的［Ca2+］升高的作用，而17β－雌二醇、孕酮、醛固酮及雄烯二酮则无此作用。10－4mol／L的RU38486可部分阻断皮质酮的抑制效应，当细胞外无钙时毒蕈也能引起［Ca2+］．升高，此效应也可被皮质酮所阻断。上述结果表明：糖度质激素抑制AMCC的激动性儿茶酚胺分泌是非基因组的，此作用经过抑制其细胞内钙升高而实现，并提示有膜受体的参与。
Secretion of catecholamines by primrily tultured rat adrenal medullary chromaffiu cells(AMCCs) in response to acetylcholine (10-5mol/L), nicotine (10-5mol/L), muscarinine (10-5mol/L) and 55mmol/L K+ in 20 min were measured by HPLC-ED in order to study the rapid effect of glucocorticoids on thestimulated secretion of catecbolamines(Dex)at 10-4mol/L and 10-5mol/L and corticostfrone at 10-5,mol/L inhibited the stimulated catecholamine secretion. 17β－estradiol and progesterone wereinhibitory at 10-5mol/L,but not at 10-7mol/L. Aldosterone, androstenedione and cholesterol had no effectS.Puromycin had no influence on the efrectS of corticosterone. In order to reveal the underlying intracellularevents accompanying secretion,the changes in intracellular calcium ([Ca2]1) were measured by Spex system. Corticosterone significantly inhibited the increase of [Ca2+]1 in response to acetylcholine, nicotine,muscarine and high K+. Dexamthasone was inhibitory, but 17β－estradiol, progesterone, aldosterone andandrostenedione did not. RU38486 at 10-4mol/L partially blocked the rapid inhibitory effect of corticosterone on setretion and [Ca2+]1. produced by ACh. The increase in [Ca2+]. by muscarine in the absence of external Ca2+ was also inhibited by corticosterone. The results Indicated that GC non-genomically inhibited thestimulated secretion of catecholamine in AMCCs by inhibiting the stimulated increase of LCa2+],suggestingthe involvement of a membrane receptor.
关键词
糖皮质激素
嗜铬细胞
细胞内钙
glucecorticoid
chromaffin cell secretion
intracellular calcium
inhibition
rapid effect
non-genomic action
high K^+
