Abstract
1 The effects of procaterol, a β2-adrenoceptor agonist, on excitatory neuro-effector transmission in the dog trachea were investigated and the findings were compared to those seen with isoprenaline, with microelectrode, double sucrose gap and tension recording methods. 2 Procaterol (10−10- 10-9 M) and isoprenaline (10−9 M) had no effect on the resting membrane potential or on the input resistance of the smooth muscle cells of dog trachea. However with increased concentrations (>10−8 M), these agents hyperpolarized the membrane and decreased the input resistance of the membrane. 3 Procaterol (10−10-10−7 M) and isoprenaline (10−9-10−7 M) dose-dependently reduced the amplitude of the twitch contractions evoked by field stimulation in the combined presence of indomethacin (10−5 M) and guanethidine (10−6 m). In parallel with actions on twitch contractions, procaterol (10−10-10−7 m) and isoprenaline (10−9-10−7 M) reduced the amplitude of the excitatory junction potentials (e.j.ps), evoked by single pulse field stimulation in the dog trachea. 4 Procaterol (10−8 M) had no effect on the post-junctional response of smooth muscle cells to exogenous acetylcholine (ACh) (10−7-10−6 M). 5 Pretreatment with ICI-118551, aβ2-adrenoceptor blocking agent, reduced the inhibitory action of procaterol on the amplitude of twitch contractions evoked by field stimulations in the dog trachea. 6 These results indicate that procaterol in low concentrations has a prejunctional action inhibiting the excitatory neuro-effector transmission in addition to a postsynaptic action, presumably by suppressing transmitter release from the vagus nerve terminals through β2-adrenoceptors in the dog tracheal tissue. The pre- and post-junctional actions of procaterol explain its potent bronchodilator effects in clinical use.

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