• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >Acid-induced modulation of airway basal tone and contractility: Role of acid-sensing ion channels (ASICs) and TRPV1 receptor
【24h】

Acid-induced modulation of airway basal tone and contractility: Role of acid-sensing ion channels (ASICs) and TRPV1 receptor

机译：酸诱导的气道基础张力和收缩性调节：酸敏感离子通道（ASICs）和TRPV1受体的作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The role of extracellular acidosis in inflammatory airway diseases is not well known. One consequence of tissue acidification is the stimulation of sensory nerves via the polymodal W-gated transmembrane channels ASICs and TRPV1 receptor. The present study investigated the effect of acidosis on airway basal tone and responsiveness in the guinea pig. Acidosis (pH 6.8, 10 min, 37 degrees C) significantly decreased the basal tone of tracheal rings (p < 0.01 vs. paired control). Moreover, pH fall raised the maximal contraction of tracheal rings to acetylcholine (p < 0.05 vs. paired control). The pH-induced relaxation of airway basal tone was inhibited by pretreatments with ASIC1a or ASIC3/ASIC2a inhibitors (0.5 MM ibuprofen, 0.1 mM gadolinium), nitric oxide synthase inhibitor (1 mM L-NAME), and guanylate cyclase inhibitor (1 mu M ODQ). In contrast, the pH-induced relaxation of airway basal tone was not modified by epithelium removal or pretreatments with a TRPV1 antagonist (1 mu M capsazepine), a combination of NK1.2.3 receptor antagonists (0.1 mu M each), a blocker of voltage-sensitive Na+ channels (1 mu M tetrodotoxin), a cyclooxygenase inhibitor with no activity on ASICs (1 mu M indomethacin) or ASIC3 and ASIC3/ASIC2b inhibitors (10 nM diclofenac, I PM aspirin). Furthermore, acid-induced hyperresponsiveness to acetylcholine was inhibited by epithelium removal, capsazepine, NK1.2.3 receptor antagonists. tetrodotoxin, amiloride, ibuprofen and diclofenac. In summary, the initial pH-induced airway relaxation seems to be independent of sensory nerves, suggesting a regulation of airway basal tone mediated by smooth muscle ASICs. Conversely, the pH-induced hyperresponsiveness involves sensory nerves-dependent ASICs and TRPV1, and an unknown epithelial component in response to acidosis. (C) 2007 Elsevier Inc. All rights reserved.
机译：细胞外酸中毒在炎性气道疾病中的作用尚不清楚。组织酸化的结果之一是通过多峰W门控跨膜通道ASIC和TRPV1受体刺激感觉神经。本研究调查了酸中毒对豚鼠气道基础张力和反应性的影响。酸中毒（pH 6.8，10分钟，37摄氏度）显着降低了气管环的基调（与配对对照相比，p <0.01）。此外，pH下降会增加气管环向乙酰胆碱的最大收缩（与配对对照相比，p <0.05）。用ASIC1a或ASIC3 / ASIC2a抑制剂（0.5 MM布洛芬，0.1 mM）），一氧化氮合酶抑制剂（1 mM L-NAME）和鸟苷酸环化酶抑制剂（1μM ODQ）。相反，通过上皮去除或用TRPV1拮抗剂（1μM capsazepine），NK1.2.3受体拮抗剂（每种0.1μM）的组合，电压的阻断剂进行的上皮去除或预处理，并未改变pH诱导的气道基础张力的松弛。敏感的Na +通道（1μM河豚毒素），一种对ASIC（1μM吲哚美辛）或ASIC3和ASIC3 / ASIC2b抑制剂（10 nM双氯芬酸，PM阿司匹林）无活性的环氧合酶抑制剂。此外，酸诱导的对乙酰胆碱的高反应性被上皮去除，capsazepine，NK1.2.3受体拮抗剂抑制。河豚毒素，阿米洛利，布洛芬和双氯芬酸。总之，最初的pH诱导的气道舒张似乎独立于感觉神经，表明由平滑肌ASIC介导的气道基础音调。相反，pH引起的反应过度涉及感觉神经依赖的ASIC和TRPV1，以及对酸中毒反应未知的上皮成分。 （C）2007 Elsevier Inc.保留所有权利。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号