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目的 研究糖皮质激素 (GC)对大鼠肾上腺髓质嗜铬细胞 (AMCC)分泌儿茶酚胺(CA)的作用机制。方法 用 5 μmol/L钙荧光染料fura 2AM负载体外培养的大鼠AMCC ,在激光扫描共聚焦显微镜 (LSCM )下实时测定地塞米松 (Dex)作用前后 ,KCl和尼古丁 (NIC)诱发细胞内[Ca2 + ] i 的变化。结果 5 0 μmol/LDex对 60mmol/LKCl诱发大鼠AMCC内 [Ca2 + ] i的变化影响不大 ,差异无显著性 (P >0 .0 5 )。 5 0 μmol/LDex对 5 0 μmol/LNIC诱发细胞内 [Ca2 + ] i的变化有明显抑制作用 ,在灌洗 5和 10min时峰值抑制率分别为 (3 2 .9± 5 .2 ) %和 (3 5 .4± 6.0 ) %。结论 GC急性作用于大鼠AMCC ,对KCl所诱发的 [Ca2 + ] i升高无明显影响 ,但能明显抑制NIC所诱发细胞内 [Ca2 + ] i的升高 ,提示GC对大鼠AMCC分泌CA的急性效应可能与NIC受体有关
Objective To study the mechanism of glucocorticoid (GC) on catecholamine (CA) secretion in rat adrenal medullary chromaffin cells (AMCC). Methods KCC and nicotine (NIC) -induced intracranial [AMCC] were induced by 5 μmol / L calcium fura 2AM in vitro. The effects of dexamethasone (Dex) Ca2 +] i changes. Results 5 μmol / L Dex had no significant effect on the changes of [Ca2 +] i in AMCC induced by 60 mmol / L KCl, but the difference was not significant (P> 0.05). 50 μmol / L Dex could significantly inhibit the change of [Ca2 +] i in 50 μmol / L LNIC induced cells, and the peak inhibition rates at 5 and 10 min were (32.9 ± 5.2)% and (3.54 ± 6.0)%. CONCLUSION: The acute effects of GC on rat AMCC have no significant effect on the increase of [Ca2 +] i induced by KCl, but can significantly inhibit the increase of [Ca2 +] i induced by NIC, suggesting that GC can inhibit the secretion of AMCC The acute effects of CA may be related to NIC receptors