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首页> 外文期刊>American Journal of Physiology >Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi.
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Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi.

机译：猪支气管forskolin诱导液体分泌的离子机制。

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摘要

cAMP-elevating agents such as forskolin and vasoactive intestinal peptide induce liquid secretion by tracheobronchial submucosal glands. This pathway is thought to be CFTR dependent and thus defective in cystic fibrosis; however, the ionic mechanism that drives this secretion process is incompletely understood. To better define this mechanism, we studied the effects of ion transport inhibitors on the forskolin-induced liquid secretion response (Jv) of porcine distal bronchi. The forskolin-induced Jv was driven by a combination of bumetanide-sensitive Cl- secretion and DIDS-sensitive HCO3- secretion. When Cl- secretion was inhibited with bumetanide, Na+/H+ exchange-dependent HCO3- secretion was apparently induced to compensate for the loss of Cl- secretion. The forskolin-induced Jv was significantly inhibited by the anion channel blockers 5-nitro-2-(3-phenylpropylamino)benzoic acid, diphenylamine-2-carboxylate, and glibenclamide. We conclude that the forskolin-induced Jv shares many characteristics of cholinergically induced secretion except for the presence of a DIDS-sensitive component. Although the identity of the DIDS-sensitive component is unclear, we speculate that it represents a basolateral membrane Na+ -HCO3- cotransporter or an Na+-dependent anion exchanger, which could account for transepithelial HCO3- secretion.
机译：cAMP增强剂（例如毛喉素和血管活性肠肽）可诱导气管支气管粘膜下腺体分泌液体。该途径被认为是CFTR依赖性的，因此在囊性纤维化中存在缺陷。但是，驱动该分泌过程的离子机制尚不完全清楚。为了更好地定义这种机制，我们研究了离子转运抑制剂对猪远侧支气管毛喉素诱导的液体分泌反应（Jv）的影响。佛司可林诱导的合资企业是由布美他尼敏感的Cl分泌和DIDS敏感的HCO3分泌共同驱动的。当布美他尼抑制Cl-分泌时，显然诱导了Na + / H +交换依赖性HCO3-分泌，以补偿Cl-分泌的损失。佛司可林诱导的Jv被阴离子通道阻滞剂5-硝基-2-（3-苯基丙基氨基）苯甲酸，二苯胺-2-羧酸盐和格列本脲显着抑制。我们得出的结论是，除了存在DIDS敏感成分外，福司柯林诱导的合资企业还具有许多胆碱能诱导分泌的特征。尽管尚不清楚DIDS敏感成分的身份，但我们推测它代表了基底外侧膜Na + -HCO3-共转运蛋白或Na +依赖性阴离子交换剂，这可能解释了上皮HCO3-的分泌。

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