Characteristics and regulation of a muscarinically activated K current in HSG-PA cells.

Characteristics and regulation of a muscarinically activated K current in HSG-PA cells.
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HSG-PA 细胞中毒蕈碱激活 K 电流的特征和调节。

DOI:
10.1152/ajpcell.1994.266.1.c58
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发表时间:
1994
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Oda,D
Oda,D
中科院分区:
--
文献类型:
--
作者:
Izutsu,KT;Fatherazi,S;Wellner,RB;Herrington,J;Belton,CM;Oda,D

文献摘要

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在毒蕈碱受体活化或暴露于已知信号传导剂后,在HSG-PA细胞(唾液腺导管细胞的拟议模型)中测量全细胞电流。暴露于卡巴胆碱或oxotremorine M产生大的,往往是振荡的外向电流的反向电位表示的K电流增加。该电流对细胞外的阿托品、蛇毒和奎宁敏感,但对apamin不敏感,对移液管中的1,2-双(2-氨基苯氧基)乙烷-N,N,N ',N'-四乙酸也不敏感。鸟苷5 '-O-(3-硫代三磷酸)延长或增加反应,并模拟D-肌肌醇1,4,5-三磷酸(IP 3)或肝素在移液管和细胞外钙离子载体。四乙铵通过毒蕈碱受体间接抑制反应。细胞悬浮液中的Fura 2表明,毒蕈碱激动剂使胞质Ca 2+浓度([Ca 2 +]i)增加5至7倍,并且在单个细胞中用indo 1进行的测量表明,外向电流的振荡变化与[Ca 2 +]i的平行变化密切相关。结果表明,毒蕈碱受体刺激HSG-PA细胞激活Ca(2+)激活的K通道,通过涉及G蛋白,IP 3的生产,并增加[Ca 2 +]i水平的信号通路。这些结果与唾液腺腺泡细胞中的结果相似。
Whole cell currents were measured in HSG-PA cells (a proposed model for salivary gland duct cells) after muscarinic receptor activation or exposure to known signaling agents. Exposure to carbachol or oxotremorine M produced large and often oscillatory increases in outward current whose reversal potentials indicated a K current. The current was sensitive to extracellular atropine, charybdotoxin, and quinine, but not apamin, and to 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid in the pipette. The response was prolonged or increased by guanosine 5'-O-(3-thiotriphosphate) and mimicked by D-myo-inositol 1,4,5-trisphosphate (IP3) or heparin in the pipette and by extracellular Ca ionophores. Tetraethylammonium indirectly inhibited the response via the muscarinic receptor. Fura 2 in cell suspensions showed that muscarinic agonists increased cytosolic Ca ion concentration ([Ca2+]i) five- to sevenfold, and measurements with indo 1 in individual cells showed that the oscillatory changes in outward current were tightly correlated with parallel changes in [Ca2+]i. The results indicate that muscarinic receptor stimulation of HSG-PA cells activates Ca(2+)-activated K channels through a signaling pathway involving a G protein, IP3 production, and increased [Ca2+]i levels. These findings are similar to those in salivary gland acinar cells.