Kinin-stimulated chloride secretion in mouse colon requires the participation of CFTR chloride channels.

The effect of lysylbradykinin on electrogenic chloride secretion in the epithelium of the mouse colon has been investigated. The peptide was active only when applied to the basolateral surface and its effects were inhibited by the B2 receptor antagonist, Hoe 140, also applied to the same surface. The chloride channel blocker, niflumic acid, also inhibited the response to kinin when added apically. Cyclo-oxygenase inhibition with piroxicam attenuated the responses to kinin, indicating involvement of prostaglandins in the responses. It is concluded that lysylbradykinin increases chloride secretion by acting via B2 receptors and, as with other tissues, brings about secretion through the agency of multiple messengers. In colonic epithelia from cystic fibrosis (CF) mice lysylbradykinin was without effect, suggesting that the final effector process involves apically located cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels.