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首页> 外文期刊>American Journal of Physiology >NO inhibits signal transduction pathway for ATP release from erythrocytes via its action on heterotrimeric G protein Gi.
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NO inhibits signal transduction pathway for ATP release from erythrocytes via its action on heterotrimeric G protein Gi.

机译：NO通过其对异源三聚体G蛋白Gi的作用，抑制了ATP从红细胞中释放的信号转导途径。

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摘要

The release of ATP from erythrocytes involves a signal transduction pathway of which cystic fibrosis transmembrane conductance regulator, PKA, adenylyl cyclase, and the heterotrimeric G proteins G(s) and G(i) are components. In the pulmonary circulation, ATP released from the erythrocyte stimulates nitric oxide (NO) synthesis, thereby regulating vascular resistance. We reported that NO liberated from an NO donor inhibited ATP release from erythrocytes in response to decreased Po(2) or mechanical deformation. Here, we investigated the hypothesis that NO inhibits ATP release from erythrocytes via inactivation of G(i). Washed rabbit erythrocytes were incubated in the presence or absence of the NO donor N-(2-aminoethyl)-N-(2-hydroxy-2-nitrosohydrazino)-1,2-ethylenediamine (spermine NONOate; 100 nM, 20 min), followed by treatment with agents that activate specific components of the signal transduction pathway promoting ATP release. Neither ATP release nor cAMP accumulation induced by either forskolin (100 microM, n = 7) or iloprost (100 nM, n = 6) was inhibited by spermine NONOate. These experiments suggest that the inhibitory action of NO is not the result of inactivation of adenylyl cyclase or G(s), respectively. However, spermine NONOate completely inhibited ATP release in response to mastoparan (10 microm, P < 0.05, n = 5), a specific activator of G(i). Spermine (100 nM, 20 min), the polyamine remaining after liberation of NO from spermine NONOate, had no affect on mastoparan-induced ATP release (n = 4). These results support the hypothesis that NO inhibits ATP release from erythrocytes via inactivation of the heterotrimeric G protein G(i).
机译：ATP从红细胞的释放涉及信号转导途径，其中囊性纤维化跨膜电导调节剂，PKA，腺苷酸环化酶和异源三聚体G蛋白G（s）和G（i）是组成部分。在肺循环中，从红细胞释放的ATP刺激一氧化氮（NO）合成，从而调节血管阻力。我们报告说，从NO供体释放的NO抑制了Po（2）降低或机械变形，从而抑制了红细胞的ATP释放。在这里，我们调查了NO抑制G（i）失活抑制红细胞ATP释放的假说。在存在或不存在NO供体N-（2-氨基乙基）-N-（2-羟基-2-亚硝基肼基）-1,2-乙二胺（精胺NONOate; 100 nM，20分钟）的情况下，将洗涤过的兔红细胞进行孵育，然后用能激活信号转导途径中促进ATP释放的特定成分的药物处理。精胺NONOate既不抑制Forskolin（100 microM，n = 7）或伊洛前列素（100 nM，n = 6）诱导的ATP释放或cAMP积累。这些实验表明，NO的抑制作用不是腺苷酸环化酶或G（s）失活的结果。但是，精胺NONOate完全响应于G（i）的特异性激活剂马托帕兰（10 microm，P <0.05，n = 5）完全抑制ATP释放。精胺（100 nM，20分钟）是NO从精胺NONOate释放出来后残留的多胺，对masoparanan诱导的ATP释放没有影响（n = 4）。这些结果支持这样的假设，即NO通过异源三聚体G蛋白G（i）的失活抑制红细胞中ATP的释放。

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