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首页> 外文期刊>American Journal of Physiology >Paracrine purinergic signaling determines lung endothelial nitric oxide production.
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Paracrine purinergic signaling determines lung endothelial nitric oxide production.

机译：旁分泌嘌呤能信号决定肺内皮一氧化氮的产生。

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摘要

Although the vascular bed is a major source of nitric oxide (NO) production, factors regulating the production remain unclear. We considered the role played by paracrine signaling. Determinations by fluorescence microscopy in isolated, blood-perfused rat and mouse lungs revealed that a brief lung expansion enhanced cytosolic Ca(2+) (Ca(2+)cyt) oscillations in alveolar epithelial (AEC) and endothelial (EC) cells, and NO production in EC. Furthermore, as assessed by a novel microlavage assay, alveolar ATP production increased. Intra-alveolar microinfusion of the purinergic receptor antagonist, PPADS, and the nucleotide hydrolyzing enzyme, apyrase, each completely blocked the Ca(2+)cyt and NO responses in EC. Lung expansion induced Ca(2+)cyt oscillations in mice lacking the P2Y1, but not the P2Y2, purinergic receptors, which were located in the perivascular interstitium basolateral to AEC. Prolonged lung expansion instituted by mechanical ventilation at high tidal volume increased EC expression of nitrotyrosine, indicating development of nitrosative stress in lung microvessels. These findings reveal a novel mechanism in which mechanically induced purinergic signaling couples cross-compartmental Ca(2+)cyt oscillations to microvascular NO production.
机译：尽管血管床是一氧化氮（NO）产生的主要来源，但尚不清楚调节该产生的因素。我们考虑了旁分泌信号传导的作用。通过荧光显微镜在孤立的，血液灌注的大鼠和小鼠肺部的测定表明，短暂的肺扩张增强了肺泡上皮（AEC）和内皮（EC）细胞中的胞质Ca（2+）（Ca（2+）cyt）振荡。 EC中不生产。此外，通过新型微灌洗法评估，肺泡ATP的产生增加。嘌呤能受体拮抗剂，PPADS和核苷酸水解酶，腺苷三磷酸酶的肺泡内微输注均完全阻断了EC中的Ca（2+）cyt和NO反应。肺膨胀在缺乏P2Y1的小鼠中引起Ca（2+）cyt振荡，但缺少P2Y2的嘌呤能受体，它们位于AEC基底外侧的血管周间质。在高潮气量下通过机械通气引起的长时间肺扩张增加了硝基酪氨酸的EC表达，表明肺微血管中亚硝化应激的发展。这些发现揭示了一种新的机制，其中机械诱导的嘌呤能信号转导跨室Ca（2+）cyt振荡到微血管NO生产。

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