酚妥拉明和育亨宾抑制ATP-sensitive K +通道在小鼠胰岛细胞。

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植物TD, Henquin JC

酚妥拉明和育亨宾抑制ATP-sensitive K +通道在小鼠胰岛细胞。

Br J杂志。1990年9月,101 (1):115 - 20。

PubMed ID

2282453 (在PubMed

]

文摘

1。酚妥拉明的影响,育亨宾对腺苷三磷酸(ATP)敏感的K +通道正常老鼠细胞进行了研究。2。在3毫米葡萄糖的存在,许多ATP-sensitive K +通道是开放的胰腺β-细胞的膜。在这些条件下,酚妥拉明抑制86 rb流出的小岛。这种抑制是快100比20 microM酚妥拉明但其稳态与浓度大小相似。育亨宾(20 - 100 microM)也抑制了射流速度,但不像酚妥拉明的。3所示。在6毫米葡萄糖的存在,大多数ATP-sensitive K +通道关闭胰腺β-细胞的膜。100年首场microM氯甲苯噻嗪显著加速86 rb射流引起的小岛。 This acceleration was almost entirely prevented by 20 microM phentolamine. It was barely affected by 20 microM yohimbine and reduced by 50% by 100 microM yohimbine. 4. ATP-sensitive K+ currents were studied in single beta-cells by the whole cell patch-clamp technique. Phentolamine (20-100 microM) caused a progressive but almost complete and irreversible inhibition of the current. The effects of yohimbine were faster but smaller; the inhibition was still incomplete with 100 microM yohimbine. 5. The increase in ATP-sensitive K+ current produced by 100 microM diazoxide was prevented by 100 microM phentolamine but only partially attenuated by 100 microM yohimbine. 6. It is concluded that phentolamine inhibits ATP-sensitive K+ channels in pancreatic beta-cells. This novel effect of phentolamine resembles that of hypoglycaemic sulphonylureas. It may account for previously unexplained effects of the drug. These observations also call for reinterpretation of many studies in which phentolamine was used as an allegedly specific blocker of alpha-adrenoceptors.

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药物靶点

药物	目标	类	生物	药理作用	行动
育亨宾	ATP-sensitive钾通道(蛋白质组)	蛋白质组	人类	未知的	抑制剂	细节