Bradykinin increased mean short-circuit (I(sc)) when added either to the mucosal (K(D) = 1.1 nM; ΔI(sc)(max) = 29.8 ± 4.4 μA/cm2) or submucosal bath (K(D) = 108 nM; ΔI(sc)(max) = 27.1 ± 4.9 μA/cm2). Bumetanide or replacement of Cl reduced the maximal change in I(sc). In paired tissues, the increase in net 36Cl flux toward the mucosa equaled the change in I(sc). Net 22Na flux toward the submucosa was unchanged. Involvement of intramural nerves was ruled out because bradykinin-induced increases in I(sc) 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 I(sc) 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.
|Original language||English (US)|
|Title of host publication||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - 1985|
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