Effects of beta-endorphin and dynorphin A on cholinergic neurotransmission in canine airway smooth muscle.

To determine the effects of the opioid peptides, beta-endorphin and dynorphin A, on airway smooth muscle function and its possible modulation by tissue peptidases, we studied canine bronchial segments under isometric conditions in vitro. Addition of beta-endorphin or dynorphin A did not alter the resting tension. However, beta-endorphin (10(-6) M) but not dynorphin A decreased the contractile responses to electrical field stimulation (EFS, 0.5-40 Hz). This effect was dose-dependent and reversed by naloxone. In contrast, acetylcholine-induced contractions were not affected by these opioids. The beta-endorphin-induced inhibition of the contractile responses to EFS was not augmented by peptidase inhibitors such as thiorphan, captopril, bestatin and leupeptin. These results suggest that beta-endorphin prejunctionally inhibits parasympathetic muscle contraction, and that endogenous peptidases do not play a modulatory role in this effect of beta-endorphin.