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首页> 外文期刊>American Journal of Physiology >Cellular mechanisms underlying cutaneous pressure-induced vasodilation: in vivo involvement of potassium channels.
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Cellular mechanisms underlying cutaneous pressure-induced vasodilation: in vivo involvement of potassium channels.

机译：皮肤压力诱导的血管舒张的基础细胞机制：体内钾通道的参与。

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摘要

In the skin of humans and rodents, local pressure induces localized cutaneous vasodilation, which may be protective against pressure-induced microvascular dysfunction and lesion formation. Once activated by the local pressure application, capsaicin-sensitive nerve fibers release neuropeptides that act on the endothelium to synthesize and release nitric oxide (NO) and prostaglandins, leading to the development of the cutaneous pressure-induced vasodilation (PIV). The present study was undertaken to test in vivo the hypothesis that PIV is mediated or modulated by differential activation of K+ channels in anesthetized rats using pharmacological methods. Local pressure was applied at 11.1 Pa/s. Endothelium-independent and -dependent vasodilation were tested using iontophoretic delivery of sodium nitroprusside (SNP) and acetylcholine (ACh), respectively, and was correlated with PIV response. PIV was reduced after systemic administration of tetraethylammonium (a nonspecific K+ channel blocker), iberiotoxin [a specific large-conductance Ca2+-activated K+ (BKCa) channel blocker], and glibenclamide [a specific ATP-sensitive K+ (KATP) channel blocker], whereas PIV was unchanged by apamin (a specific small-conductance Ca2+-activated K+ channel blocker) and 4-aminopyridine (a specific voltage-sensitive K+ channel blocker). The responses to SNP and ACh were reduced by iberiotoxin but were unchanged by glibenclamide. We conclude that the cellular mechanism of PIV in skin involves BKCa and KATP channels. We suggest that the opening of BKCa and KATP channels contributes to the hyperpolarization of vascular smooth muscle cells to produce PIV development mainly via the NO and prostaglandin pathways, respectively.
机译：在人类和啮齿动物的皮肤中，局部压力会引起局部皮肤血管舒张，这可能会对压力引起的微血管功能障碍和病变的形成起到保护作用。对辣椒素敏感的神经纤维一旦被局部压力作用激活，就会释放作用于内皮的神经肽，从而合成并释放一氧化氮（NO）和前列腺素，从而导致皮肤压力诱导的血管舒张（PIV）的发展。进行本研究以在体内测试以下假设：使用药理学方法，麻醉大鼠体内KIV通道的差异激活介导或调节了PIV。以11.1Pa / s施加局部压力。分别使用硝普钠（SNP）和乙酰胆碱（ACh）的离子电渗疗法测试了内皮依赖性和依赖性血管舒张，并与PIV反应相关。全身性给予四乙铵（一种非特异性K +通道阻滞剂），埃博毒素（一种特定的大电流Ca2 +活化的K +（BKCa）通道阻滞剂）和格列本脲[一种特定的ATP敏感性K +（KATP）通道阻滞剂]全身给药后，PIV降低，而apamin（一种特定的小电导Ca2 +激活的K +通道阻滞剂）和4-氨基吡啶（一种特定的电压敏感的K +通道阻滞剂）的PIV不变。 iberiotoxin降低了对SNP和ACh的反应，但格列本脲未改变。我们得出结论，皮肤中PIV的细胞机制涉及BKCa和KATP通道。我们建议，BKCa和KATP通道的开放有助于血管平滑肌细胞的超极化，分别主要通过NO和前列腺素途径产生PIV发育。

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