Stimulation of adenosine receptor enhances α1 ‐adrenergic receptor‐mediated activation of phospholipase C and Ca2+ mobilization in a pertussis toxin‐sensitive manner in FRTL‐5 thyroid cells
Stimulation of adenosine receptor enhances α1 ‐adrenergic receptor‐mediated activation of phospholipase C and Ca2+ mobilization in a pertussis toxin‐sensitive manner in FRTL‐5 thyroid cells
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刺激腺苷受体可增强 FRTL-5 甲状腺细胞中 α1 肾上腺素能受体介导的磷脂酶 C 激活和 Ca2+ 以百日咳毒素敏感方式的动员
DOI：
10.1016/0014-5793(89)80450-8
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发表时间：
1989
期刊：
影响因子：
3.5
通讯作者：
Y. Kondo
中科院分区：
文献类型：
--
作者：
F. Okajima;Koichi Sato;K. Sho;Y. Kondo
去甲肾上腺素（NE）通过α1-肾上腺素能受体刺激FRTL-5甲状腺细胞，引起胞浆内Ca ~（2+）（[Ca ~（2+）]i）动员和磷脂酶C激活。腺苷及其受体激动剂苯异丙基腺苷（PIA），虽然没有发挥直接作用，显着增强NE引起的变化。基础NE行动没有完全取消，而腺苷和PIA的许可行动被完全取消的细胞与胰岛活化蛋白（IAP），百日咳毒素预处理。腺苷或PIA诱导的cAMP水平降低不是其容许效应的原因，因为这种效应不能通过添加cAMP增加剂逆转。我们的结论是IAP底物GTP结合蛋白在腺苷受体和α1-肾上腺素能受体偶联磷脂酶C系统之间形成刺激偶联中起着新的作用。
Norepinephrine (NE) stimulated FRTL-5 thyroid cells via an α1-adrenergic receptor, resulting in cytosolic Ca2+([Ca2+]i) mobilization and activation of phospholipase C. Adenosine and its receptor agonist, phenylisopropyladenosine (PIA), although not exerting a direct effect, markedly enhanced the NE-induced changes. Basal NE action was not totally abolished whereas the permissive action of adenosine and PIA was completely abolished by pretreatment of the cells with islet-activating protein (IAP), pertussis toxin. The decrease in cAMP level induced by adenosine or PIA is not the cause of their permissive effect, since this effect was not reversed by the addition of cAMP-increasing agents. We conclude that an IAP substrate GTP-binding protein(s) plays a novel role in forming a stimulatory coupling between an adenosine receptor and an α1-adrenergic receptor-coupled phospholipase C system.