Mechanisms of intrinsic force in small human airways

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• 作者：Mark E. Wylam^a ; ^{wylam.mark@mayo.edu} ; Ailing Xue^a ; Gary C. Sieck^b
• 关键词：Intrinsic force ; Human ; Airway smooth muscle ; Asthma ; Intracellular calcium concentration [Ca2+]i
• 刊名：Respiratory Physiology & Neurobiology
• 出版年：2012
• 期刊代码：185_15699048
• 类别：bio
• 出版时间：15 April, 2012
• 卷：181
• 期：1
• 页码：99-108
• 文件大小：752 K

摘要

We quantified the magnitude and investigated mechanisms regulating intrinsic force (IF) in human airway smooth muscle (hASM). IF was identified by reducing extracellular calcium (Ca²⁺) concentration to nominally zero in freshly isolated isometrically mounted 2 mm human bronchi. Our results show: (1) the magnitude of IF is 鈭?0%of the maximal total force elicited by acetylcholine (10^鈭? M) and is epithelial independent, (2) IF can also be revealed by 尾-adrenergic activation (isoproterenol), non-specific cationic channel blockade (La³⁺) or L-type voltage gated Ca²⁺ channel blockade (nifedipine), (3) atropine, indomethacin, AA-861, or pyrilamine did not affect IF, (4) IF was reduced by the intracellular Ca²⁺ ([Ca²⁺]_i) chelating agent BAPTA-AM, (5) 蠅-conotoxin had no effect on IF. In studies in cultured hASM cells nominally zero Ca²⁺ buffer and BAPTA-AM reduced [Ca²⁺]_i but isoproterenol and nifedipine did not. Taken together these results indicate that rapid reduction of [Ca²⁺]_i reveals a permissive relationship between extracellular Ca²⁺, [Ca²⁺]_i and IF. However IF can be dissipated by mechanisms effecting Ca²⁺ sensitivity. We speculate that an increase of IF, a fundamental property of ASM, could be related to human airway clinical hyperresponsiveness and must be accounted for in in vitro studies of hASM.