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首页> 外文期刊>Cellular Physiology and Biochemistry >Diadenosine polyphosphates activate a Ca2+-dependent K+-conductance in porcine aortic smooth muscle cells via P2-purinoceptors
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Diadenosine polyphosphates activate a Ca2+-dependent K+-conductance in porcine aortic smooth muscle cells via P2-purinoceptors

机译：腺苷多磷酸通过P2-嘌呤受体激活猪主动脉平滑肌细胞中Ca2 +依赖性的K +传导。

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摘要

Effects of the diadenosine polyphosphates P-1,P-3-diadenosine triphosphate (Ap3A), P-1,P-4-diadenosine tetraphosphate (Ap4A), P-1,P-5-diadenosine pentaphosphate (Ap5A) and P1,PG-diadenosine hexaphosphate (Ap6A) and of adenosine, ATP, ADP AMP, UTP on smooth muscle cells from porcine aorta were examined. Membrane voltages and cellular conductances were measured in the slow whole cell configuration of the patch clamp technique. All four diadenosine polyphosphates, adenosine, AMP and ADP predominantly hyperpolarized membrane voltages with only occasional transient initial depolarizations whereas ATP and UTP led to sustained depolarizations. All four diadenosine polyphosphates increased cellular conductances. The effects of Ap5A on membrane voltages were almost completely inhibited by the putative P2-purinoceptor antagonist pyridoxal-phosphate-6-azophenyl-2',4'-di acid (PPADS, 10 mu mol/l) and only partially reduced by the putative A(2)-purinoceptor antagonist 3,7-dimethyl-1-propragyl-xanthine (DMPX, 10 mu mol/l) or the Ap4A-receptor antagonist diinosine pentaphosphate (Ip5I, 10 mu mol/l). The adenosine-induced hyperpolarization was partially reduced by the putative A,-purinoceptor antagonist 8-cyclopentyl-1,3-dipropargylxanthine (DPCPX, 0.1 mu mol/l) or by DMPX while PPADS or Ip5I were without effects. Ap5A-induced hyperpolarizations were inhibited by Ba2+ and clotrimazole but not by glibenclamide. We conclude that diadenosine polyphosphates activate predominantly a Ca2+-dependent K+-conductance in smooth muscle cells obtained from porcine aorta most likely mediated via P2Y-purinoceptors and possibly partially also by Ap4A receptors. Copyright (C) 2000 S. Karger AG, Baser. [References: 38]
机译：磷酸腺苷多磷酸P-1，P-3-腺苷三磷酸（Ap3A），P-1，P-4-腺苷四磷酸（Ap4A），P-1，P-5-腺苷五磷酸（Ap5A）和P1，PG检验了猪主动脉平滑肌细胞上的β-重氮腺苷六磷酸（Ap6A）和腺苷，ATP，ADP AMP，UTP。在膜片钳技术的慢速全电池配置中测量膜电压和细胞电导。四种腺苷多磷酸盐，腺苷，AMP和ADP均主要为超极化膜电压，仅偶尔出现短暂的初始去极化，而ATP和UTP导致持续去极化。所有四种聚腺苷多磷酸都增加了细胞电导。假定的P2-嘌呤受体拮抗剂吡ido醛-磷酸盐-6-偶氮苯基-2'，4'-二酸（PPADS，10μmol / l）几乎完全抑制了Ap5A对膜电压的影响，而仅被假定的部分降低了A（2）-嘌呤受体拮抗剂3,7-二甲基-1-丙酰基黄嘌呤（DMPX，10μmol/ l）或Ap4A-受体拮抗剂二肌苷五磷酸（Ip5I，10μmol/ l）。假定的A，嘌呤受体拮抗剂8-环戊基-1,3-二炔丙基黄嘌呤（DPCPX，0.1μmol / l）或DMPX可以部分降低腺苷诱导的超极化，而PPADS或Ip5I没有作用。 Ap5A诱导的超极化受到Ba2 +和克霉唑的抑制，但不受glibenclamide的抑制。我们得出结论，在从猪主动脉获得的平滑肌细胞中，腺苷多磷酸主要激活Ca2 +依赖性的K +传导，最有可能通过P2Y-嘌呤受体介导，也可能部分由Ap4A受体介导。版权所有（C）2000 S. Karger AG，Baser。 [参考：38]

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