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Am J Physiol Lung Cell Mol Physiol 278: L485-L491, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 3, L485-L491, March 2000

Effect of bradykinin on membrane properties of guinea pig bronchial parasympathetic ganglion neurons

Radhika Kajekar and Allen C. Myers

Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland 21224

The effect of bradykinin on membrane properties of parasympathetic ganglion neurons in isolated guinea pig bronchial tissue was studied using intracellular recording techniques. Bradykinin (1-100 nM) caused a reversible membrane potential depolarization of ganglion neurons that was not associated with a change in input resistance. The selective bradykinin B2 receptor antagonist HOE-140 inhibited bradykinin-induced membrane depolarizations. Furthermore, the cyclooxygenase inhibitor indomethacin attenuated bradykinin-induced membrane depolarizations to a similar magnitude (~70%) as HOE-140. However, neurokinin-1 and -3 receptor antagonists did not have similar inhibitory effects. The ability of bradykinin to directly alter active properties of parasympathetic ganglion neurons was also examined. Bradykinin (100 nM) significantly reduced the duration of the afterhyperpolarization (AHP) that followed four consecutive action potentials. The inhibitory effect of bradykinin on the AHP response was reversed by HOE-140 but not by indomethacin. These results indicate that bradykinin can stimulate airway parasympathetic ganglion neurons independent of sensory nerve activation and provide an alternative mechanism for regulating airway parasympathetic tone.

autonomic ganglia; airway; sensory nerves; intracellular recording; cyclooxygenase.


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