Bradykinin stimulates Cl secretion and prostaglandin E2 release by canine tracheal epithelium.
Bradykinin stimulates Cl secretion and prostaglandin E2 release by canine tracheal epithelium.
复制标题
缓激肽刺激犬气管上皮的 Cl 分泌和前列腺素 E2 释放。
DOI：
10.1152/ajprenal.1985.248.1.f48
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Widdicombe,JH
中科院分区：
文献类型：
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作者：
Leikauf,GD;Ueki,IF;Nadel,JA;Widdicombe,JH
当将缓激肽添加到粘膜（KD = 1.1 nM; Δ Imaxsc = 29.8 +/- 4.4 microA/cm 2）或粘膜下浴（KD = 108 nM; Δ Imaxsc = 27.1 +/- 4.9 microA/cm 2）时，缓激肽增加平均短路电流（Isc）。布美他尼或取代Cl降低了Isc的最大变化。在配对组织中，净36 Cl流向粘膜的增加等于Isc的变化。净22 Na流向粘膜下层不变。由于缓激肽诱导的Isc增加不受酚妥拉明、普萘洛尔、阿托品或河豚毒素的抑制，因此排除了壁内神经的参与。缓激肽对上皮细胞的直接作用也可能由特异性缓激肽结合位点的放射自显影证明。花生四烯酸代谢拮抗剂吲哚美辛和二十碳-5，8，11，14-四炔酸可抑制缓激肽引起的Isc增加。最后，前列腺素E2的释放显着增加粘膜下添加缓激肽，这种效果被取消的吲哚美辛预处理。我们的结论是缓激肽刺激氯分泌犬气管上皮细胞增加前列腺素的释放。
Bradykinin increased mean short-circuit current (Isc) when added either to the mucosal (KD = 1.1 nM; delta Imaxsc = 29.8 +/- 4.4 microA/cm2) or submucosal bath (KD = 108 nM; delta Imaxsc = 27.1 +/- 4.9 microA/cm2). Bumetanide or replacement of Cl reduced the maximal change in Isc. In paired tissues, the increase in net 36Cl flux toward the mucosa equaled the change in Isc. Net 22Na flux toward the submucosa was unchanged. Involvement of intramural nerves was ruled out because bradykinin-induced increases in Isc were not inhibited by phentolamine, propranolol, atropine, or tetrodotoxin. A direct action of bradykinin on the epithelium was also made probable by the autoradiographic demonstration of specific bradykinin binding sites. The antagonists of arachidonic acid metabolism, indomethacin and eicosa-5,8,11,14-tetraynoic acid, inhibited the increase in Isc induced by bradykinin. Finally, prostaglandin E2 release was significantly increased by submucosal addition of bradykinin, and this effect was abolished by pretreatment with indomethacin. We conclude that bradykinin stimulates Cl secretion in canine tracheal epithelium by increasing prostaglandin release.