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首页> 外文期刊>The journal of sexual medicine >H 2S Relaxes Vas Deferens Smooth Muscle by Modulating the Large Conductance Ca 2+-Activated K + (BK Ca) Channels via a Redox Mechanism
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H 2S Relaxes Vas Deferens Smooth Muscle by Modulating the Large Conductance Ca 2+-Activated K + (BK Ca) Channels via a Redox Mechanism

机译：H 2S通过氧化还原机制通过调节大电导Ca 2+激活的K +（BK Ca）通道来放松Vas延缓平滑肌

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Introduction. Hydrogen sulfide (H 2S) is generated in mammalian cells mainly by one of the two pyridoxal-5′-phosphate-dependent enzymes, cystathione-γ-lyase (CSE), and cystathione-β-synthase (CBS) using L-cysteine as the main substrate. In previous studies, we found that CBS and CSE were functionally expressed in vas deferens (VD) and H 2S-mediated VD smooth muscle relaxation. However, the detail mechanisms that H 2S-relaxed VD smooth muscle were unknown so far. Aim. The aim of this study is to explore the molecular target sites of H 2S in VD smooth muscle. Methods. Isolated rat VD smooth muscle strips were used for tension recording in vitro. Double immunofluorescence staining was used to identify the localization of large conductance Ca 2+-activated K + (BK Ca) channels. Main Outcome Measures. Changes in tonic contraction of isolated rat VD smooth muscle strip were measured after the treatment of drugs. The expression of BKca channels in rat VD smooth muscle cells was also assessed. Results. The results showed that L-NG-nitroarginine methyl ester (a nitric oxide synthase inhibitor) did not affect the response of VD to sodium hydrosulphide (NaHS), suggesting that nitric oxide pathway was not involved. Further studies revealed that transient receptor potential (TRP) channels did not contribute to the NaHS-induced relaxant effect. Glibenclamide, an ATP-sensitive K channel blocker, did the same thing, whereas BK Ca channel blockers iberiotoxin or tetraethylammonium largely reversed the relaxant effect, suggesting that H 2S may target BK Ca channels. We also confirmed that BK Ca channels were localized in VD smooth muscle cells. Then, studies revealed that NaHS-induced VD smooth muscle relaxation was abolished by N-ethylmaleimide, which was widely used as a sulfhydryl alkylation compound protecting thiols from oxidation, whereas DL-Dithiothreitol, a strong reducing agent, did not affect the response of VD to NaHS. Conclusions. We concluded that H 2S relaxed the VD smooth muscle by targeting BK Ca channels via redox-mediated mechanism.
机译：介绍。硫化氢（H 2S）主要通过两种吡ido醛5'-磷酸依赖酶，胱硫醚-γ-裂合酶（CSE）和胱硫醚-β-合酶（CBS）中的一种以L-半胱氨酸为原料在哺乳动物细胞中生成。主基板。在以前的研究中，我们发现CBS和CSE在输精管（VD）和H 2S介导的VD平滑肌松弛中功能性表达。但是，至今尚不清楚H 2S松弛VD平滑肌的详细机制。目标。这项研究的目的是探索VD平滑肌中H 2S的分子靶位。方法。分离的大鼠VD平滑肌条用于体外张力记录。双重免疫荧光染色用于鉴定大电导Ca 2+激活的K +（BK Ca）通道的定位。主要观察指标。药物治疗后，测定离体大鼠VD平滑肌条的张力收缩变化。还评估了大鼠VD平滑肌细胞中BKca通道的表达。结果。结果表明，L-NG-硝基精氨酸甲酯（一氧化氮合酶抑制剂）不影响VD对氢硫化钠（NaHS）的响应，表明不涉及一氧化氮途径。进一步的研究表明，瞬时受体电位（TRP）通道对NaHS诱导的松弛作用没有贡献。格列本脲是一种对ATP敏感的K通道阻滞剂，其作用相同，而BK Ca通道阻滞剂埃博毒素或四乙铵在很大程度上逆转了松弛作用，表明H 2S可能靶向BK Ca通道。我们还证实BK Ca通道位于VD平滑肌细胞中。然后，研究表明，N-乙基马来酰亚胺消除了NaHS引起的VD平滑肌松弛，N-乙基马来酰亚胺被广泛用作巯基烷基化化合物，可保护硫醇免受氧化，而强还原剂DL-二硫苏糖醇则不影响VD的反应。到NaHS。结论。我们得出的结论是，H 2S通过氧化还原介导的机制靶向BK Ca通道来放松VD平滑肌。

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