EFFECTS OF ENZYME INHIBITORS ON JUNCTION POTENTIALS IN RESPONSE TO ADRENERGIC NERVE STIMULATION

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Recent electrophysiological and anatomical studies on transmission between the sympathetic nerve and smooth muscle have confirmed the important role of a chemical substance acting in a manner similar to the chemical substance concerned with transmission between somatic nerve and skeletal muscle. A low frequency stimulation of the hypogastric nerve produced junction potentials on the smooth muscle of the vas deferens (1) and seminal vesicle (2) in the guinea-pig. The junction potentials may be due to the release of noradrenaline from the sympathetic nerve terminals, and this conjecture is supported by the following evidence. 1) The junction potentials were strongly depressed by pretreatment or intravenous injection of reserpine (3, 4), 2) The junction potentials were also depressed by guanethidine, bretylium and high doses of various α-blocking agents, such as phenoxybenzamine, phentolamine and yohimbine (5), 3) The intravenous injection of noradrenaline induced a burst of action potentials in smooth muscle which was associated with tetanic contraction (6), 4) Many investigators (7, 8) have demonstrated pharmacologically that the nature of the contractile response of the vas deferens to hypogastric nerve stimulation was probably of sympathetic origin, 5) The guinea-pig vas deferens and seminal vesicle contain a large amount of noradrenaline and also abundant noradrenaline containing fibers which have been observed among the smooth muscle cells (9, 10). On the other hand, it is well known that monoamine oxidase (MAO) and catecholO-methyl transferase (COMT) degrade noradrenaline to deaminated and methylated metabolites. However, there are a few inconsistent results concerning the effect of MAO inhibitor on the contractile response of the guinea-pig vas deferens to hypogastric nerve stimulation. For instance, Kamijo et al. (11) and Brown and Gillespie (12) have assumed that MAO inhibitors do not potentiate the effect of catecholamine released by nerve smonoamine oxidase and catechol-O-methyl transferase on the junction potential recorded from the guinea-pig seminal vesicle in response to hypogastric nerve stimulatiotimulation, whereas Bhargava et al. (13) have observed that MAO inhibitors, such as pheniprazine and tranylcypromine, and a COMT inhibitor, pyrogallol, potentiated the contractile response of the guinea-pig vas deferens to hypogastric nerve stimulation. The present study was, therefore, undertaken to examine the effect of inhibition of monoamine oxidanse and catechol-O-methyo transferase on the iunction potential recorded from the guinea-pig seminal vesicle in response to hypogastric nerve stimulation.
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EFFECTS OF ENZYME INHIBITORS ON JUNCTION POTENTIALS IN RESPONSE TO ADRENERGIC NERVE STIMULATION

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