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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。
In order to study the rapid effect of glucocorticoid on catecholamines induced by stimulated primary adrenal chromaffin cells (AMCC) in rats, the levels of acetylcholine (10-5mol / L), nicotine (10-5mol / L), muscarinic (10-5mol / L) and 55mmol / L KCl in 20min caused by the amount of catecholamines. Dexamethasone (Dex, 10-4mol / L and 10-5mol / L) and corticosterone (10-5mol / L) can inhibit the secretion of catecholamine in AMCC; 10-7mol / L 17β-estradiol can not inhibit, 10-5mol / L can inhibit its secretion; aldosterone, androstenedione and cholesterol did not inhibit the effect. In order to reveal the intracellular changes associated with secretion, intracellular calcium ([Ca2 +]) levels were examined using the SPex detection system. Dexamethasone and corticosterone were found to inhibit the increase of [Ca2 +] caused by acetylcholine, nicotine, muscarinic and high K +, whereas 17β-estradiol, progesterone, aldosterone and androstenedione did not This role. RU38486 at 10-4 mol / L partially blocked the inhibitory effect of corticosterone, which caused [Ca2 +] when extracellular calcium was added. Increased, this effect can be blocked by corticosterone. The above results indicate that glucocorticoids inhibit the secretion of excitatory catecholamines in AMCC is non-genomic, and this effect is achieved by inhibiting the increase of intracellular calcium, suggesting the involvement of membrane receptors.