Abstract
In the isolated guinea‐pig bronchus, the potassium channel blocking agent 4‐aminopyridine (10‐4M) caused a contraction which was abolished by capsaicin tachyphylaxis, suggesting involvement of sensory neuropeptides. Charybdotoxin (10‐8, 5 × 10‐8M), which is a potent blocker of the high‐conductance Ca2+‐activated K+channel in smooth muscle, caused slowly developing and long lasting bronchoconstriction, which was resistant to capsaicin tachyphylaxis. Neither 4‐aminopyridine (10‐3, 10‐4M) nor charybdotoxin (10‐8, 5 × 10‐8M) had any significant effect on the bronchoconstriction induced by electrical field stimulation. Furthermore, charybdotoxin had no significant influence on the inhibitory effect of the α2‐adrenoceptor agonist SKF 35886 (5 × 10‐7M) on the bronchoconstriction induced by electrical field stimulation. In the isolated perfused guinea‐pig lung, 4‐aminopyridine (3 × 10‐5‐10‐3M) caused bronchoconstriction and enhanced both basal and (at 3 × 10‐5M) vagal nerve stimulation‐evoked calcitonin gene‐related peptide outflow from pulmonary sensory nerves. In conclusion, 4‐aminopyridine stimulated capsaicin‐sensitive sensory neurons and enhanced the sensory activation induced by vagal nerve stimulation in guinea‐pig lung. Charybdotoxin, on the other hand, caused bronchial contraction independently of capsaicin‐sensitive nerves.

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