Effects of procaterol, a beta-2-adrenoceptor stimulant, on neuroeffector transmission in human bronchial tissue.

It has been reported that low concentrations of noradrenaline or isoprenaline reduce the resting tension of the smooth muscle cells and suppress acetylcholine release from the vagal nerve terminals through activation of beta 2-adrenoceptors. Procaterol, beta 2-adrenoceptor stimulant, has a high potency and selectivity for airway smooth muscle tissues. However, there is little documentation on the prejunctional actions of this chemical in airway smooth muscle, especially in man. In the present study, the effects of procaterol on excitatory neuroeffector transmission in the human bronchus were investigated. Procaterol (10(-10) to 10(-7) M) dose dependently reduced the amplitude of the contractions evoked by electrical field stimulation in the presence of indomethacin (10(-5) M), FPL-55712 (10(-6) M), and guanethidine (10(-6) M). By contrast, procaterol (10(-10) to 10(-9) M) had no effect on the postjunctional response of smooth muscle cells to exogenously applied acetylcholine. Pretreatment with ICI-118551 (10(-7) M), a beta 2-adrenoceptor-blocking agent, reduced the inhibitory action of procaterol on the amplitude of twitch contractions evoked by field stimulations in the human bronchus. These results indicate that procaterol at low concentrations has a prejunctional action, inhibiting the excitatory neuroeffector transmission and presumably suppressing transmitter release from the vagal nerve terminals through beta 2-adrenoceptors in the human bronchial tissue. The prejunctional action of procaterol explains partly its potent bronchodilator effects in clinical use.