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首页> 外文期刊>Nucleosides, nucleotides and nucleic acids >Decreased ecto-NTPDase1/CD39 activity leads to desensitization of P2 purinoceptors regulating tonus of corpora cavernosa in impotent men with endothelial dysfunction.
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Decreased ecto-NTPDase1/CD39 activity leads to desensitization of P2 purinoceptors regulating tonus of corpora cavernosa in impotent men with endothelial dysfunction.

机译:ecto-NTPDase1 / CD39活性降低导致无功能的男性无血管内皮功能的P2嘌呤受体脱敏,调节海绵体的张力。

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摘要

Vascular responses to adenine nucleotides in human corpora cavernosa from men with vasculogenic erectile dysfunction were investigated. We also evaluated the catabolism of extracellular adenine nucleotides to probe its relevance to vascular hemodynamics in impotent men. Human corpora cavernosa have high NTPDase1/CD39 activity, converting ATP directly into AMP, without significant ADP formation. Extracellular ATP hydrolysis is slower in impotent patients. Adenine nucleotides have dual roles on phenylephrine-contracted strips of corpora cavernosa operated by P2X-contractant and P2Y-relaxant receptors. Prolonged exposure to endogenous ATP related to decreased NTPDase1/CD39 activity leads to P2-purinoceptor desensitization in impotent men. Shutting down ATP signaling in vasculogenic impotent men may represent a defense mechanism for preventing purinergic overstimulation.
机译:研究了血管源性勃起功能障碍男性对人海绵体中腺嘌呤核苷酸的血管反应。我们还评估了胞外腺嘌呤核苷酸的分解代谢,以探究其与无力男性的血管血流动力学的相关性。人海绵体具有高NTPDase1 / CD39活性,可将ATP直接转化为AMP,而不会形成明显的ADP。阳o患者的细胞外ATP水解较慢。腺嘌呤核苷酸在由P2X和P2Y松弛受体操纵的肾上腺素收缩的海绵体条上具有双重作用。长期暴露于与内源性ATP相关的NTPDase1 / CD39活性降低会导致阳萎男性的P2-嘌呤受体脱敏。在血管生成无能的男性中关闭ATP信号传导可能是预防嘌呤能过度刺激的防御机制。

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