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首页> 外文期刊>American Journal of Physiology >Reactive oxygen species from smooth muscle mitochondria initiate cold-induced constriction of cutaneous arteries.
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Reactive oxygen species from smooth muscle mitochondria initiate cold-induced constriction of cutaneous arteries.

机译：平滑肌线粒体中的活性氧引发冷诱导的皮肤动脉收缩。

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Cold constricts cutaneous blood vessels by selectively increasing the activity of smooth muscle alpha2-adrenoceptors (alpha2-ARs). In mouse tail arteries, alpha2-AR constriction is mediated by alpha2A-ARs at 37 degrees C, whereas the cold-induced augmentation in alpha2-AR activity is mediated entirely by alpha2C-ARs. Cold causes translocation of alpha2C-ARs from the trans-Golgi to the plasma membrane, mediated by cold-induced activation of RhoA and Rho kinase. The present experiments analyzed the mechanisms underlying these responses. Mouse tail arteries were studied in a pressure myograph. Cooling the arteries (28 degrees C) caused a rapid increase in reactive oxygen species (ROS) in smooth muscle cells, determined by confocal microscopy of arteries loaded with the ROS-sensitive probes, dichlorodihydrofluorescein or reduced Mitotracker Red. The inhibitor of mitochondrial complex I rotenone (10 micromol/l), the antioxidant N-acetylcysteine (NAC; 20 mmol/l), or the cell-permeable mimic of superoxide dismutase MnTMPyP (50 micromol/l) did not affect vasoconstriction to alpha2-AR stimulation (UK-14304) at 37 degrees C but dramatically inhibited the response at 28 degrees C. Indeed, these ROS inhibitors abolished the cold-induced increase in alpha2-AR constrictor activity. NAC (20 mmol/l) or MnTMPyP (50 micromol/l) also abolished the cold-induced activation of RhoA in human cultured vascular smooth muscle cells and the cold-induced mobilization of alpha2C-ARs to the cell surface in human embryonic kidney 293 cells transfected with the receptor. The combined results suggest that cold-induced constriction is mediated by redox signaling in smooth muscle cells, initiated by mitochondrial generation of ROS, which stimulate RhoA/Rho kinase signaling and the subsequent mobilization of alpha2C-ARs to the cell surface. Altered activity of ROS may contribute to cold-induced vasospasm occurring in Raynaud's phenomenon.
机译：感冒通过选择性增加平滑肌α2-肾上腺素能受体（alpha2-ARs）的活动来收缩皮肤血管。在小鼠尾动脉中，α2-AR收​​缩是由37度的α2A-AR介导的，而冷诱导的α2-AR活性增强完全由α2C-AR介导。感冒引起α2C-ARs从反式高尔基体向质膜的易位，其受冷诱导的RhoA和Rho激酶的激活介导。本实验分析了这些反应的潜在机制。在压力肌电图仪中研究了小鼠尾动脉。冷却动脉（28摄氏度）会导致平滑肌细胞中活性氧（ROS）的快速增加，这是通过共聚焦显微镜检查的，其中装有ROS敏感探针，二氯二氢荧光素或还原的Mitotracker Red。线粒体复合物I鱼藤酮的抑制剂（10 micromol / l），抗氧化剂N-乙酰半胱氨酸（NAC; 20 mmol / l）或超氧化物歧化酶MnTMPyP的细胞渗透性模拟物（50 micromol / l）均不影响对α2的血管收缩-AR刺激（UK-14304）在37摄氏度时可显着抑制28摄氏度时的反应。的确，这些ROS抑制剂消除了冷诱导的α2-AR收​​缩子活性的增加。 NAC（20 mmol / l）或MnTMPyP（50 micromol / l）还取消了人类培养的血管平滑肌细胞中RhoA的冷诱导激活以及α2C-ARs的冷诱导动员至人类胚胎肾脏293的细胞表面。被受体转染的细胞。综合结果表明，冷诱导的收缩由平滑肌细胞中的氧化还原信号传导介导，由线粒体产生ROS引发，ROS刺激RhoA / Rho激酶信号传导以及随后的alpha2C-ARs迁移至细胞表面。 ROS活性的改变可能有助于在雷诺现象中发生冷诱导的血管痉挛。

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