Abstract

Luminal addition of bradykinin (BK) to the open-circuited canine tracheal epithelium produces a biphasic response in transmucosal potential difference (P.D.): a rapid, transient decrease (dip) followed by a subsequent, more sustained increase (rise), both phases being associated with an increase in conductance. We have attempted to characterise the receptor subtype mediating the bradykinin response. Lys-bradykinin (Lys-BK) elicited a similar response, and its EC 50 as judged from concentration-response relations was similar to that of BK. Cross-tachyphylaxis between the two peptides confirmed a common receptor. Des-Arg 9-BK (a B 1-agonist) neither elicited a response nor inhibited responses to BK. The novel B 2-antagonist [Thi 6,9- d-Phe 8]kallidin reversibly inhibited responses to both BK and Lys-BK. The rapid changes in P.D. (dips) were unaffected by Na + removal, but were eliminated by replacing luminal Cl − with isethionate. Thus, BK, acting on B 2-receptors, transiently increases anion permeability of the luminal membrane of the canine tracheal epithelium.

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