SUMMARYNeuro-effector transmission in the smooth muscle layer of the dog trachea was studied in vitro using the micro-electrode and double sucrose gap methods.

SUMMARYEffects of prostaglandins (PGs) on the neuromuscular junction of the guinea-pig vas deferens were investigated by the micro-electrode and double sucrose gap methods.1. PGE1, PGE2 or PGF20 (10-10 to 10-7 g/ml.) did not change the membrane potential, membrane resistance and electrical threshold required to produce the action potential.2. PGs markedly suppressed the amplitude of excitatory junction potential (e.j.p.) but the facilitation phenomena seen with repetitive stimulation were not affected. PGs did not change the amplitude and frequency of the miniature e.j.p.3. The action potential recorded from the small nerve bundle with the aid of an extracellular micro-electrode method was not affected by PGs. 4. 6. Indomethacin (10-6 g/ml.) had no effect on the amplitudes of e.j.p. produced by repetitive stimulation.7. These results indicate that a low concentration of PGs interact with [Ca]o at the activated nerve terminals, but that there is no modification of the actions of Ca in the nerve terminals required for release of chemical transmitter.

Effects of noradrenaline or isoprenaline on the membrane and contractile properties of the smooth muscle cell, or on the excitatory neuro‐effector transmission in the dog trachea, in vitro, were observed by use of microelectrodes and double sucrose gap methods. Noradrenaline (<5 × 10−6 m) or isoprenaline (< 5 × 10−7 m) modified neither the membrane potential nor the membrane resistance. Increased concentrations of noradrenaline (> 5 × 10−5 m) depolarized and isoprenaline (> 5 × 10−7 m) hyperpolarized the membrane, and these actions were suppressed by phentolamine and propranolol respectively. Both catecholamines reduced the membrane resistance. Noradrenaline (5 × 10−6 m) or isoprenaline (5 × 10−7 m) reduced the resting tension, raised the mechanical threshold required to produce the contraction and suppressed the amplitude of phasic contractions evoked by electrical depolarization of the membrane. The action potential evoked by an outward current pulse in the presence of tetraethylammonium (TEA) was not affected by 5 × 10−6m isoprenaline, while the mechanical response was markedly suppressed. The excitatory junction potential (e.j.p.) evoked by electrical field stimulation was blocked by atropine. Noradrenaline (5 × 10−7 m) or isoprenaline (5 × 10−8 m) suppressed the amplitude of e.j.p. with no change in the membrane potential or input membrane resistance. Depression in the amplitude of e.j.ps produced by noradrenaline or isoprenaline reduced the amplitude of phasic contractions evoked by e.j.ps. These inhibitory actions of the catecholamines on mechanical responses and on e.j.ps were suppressed by pretreatment with propranolol (4 × 10−6 m). Dog tracheal smooth muscles are innervated by cholinergic excitatory and adrenergic inhibitory systems. Electrical field stimulation produced excitation of both cholinergic and adrenergic nerve fibres, and propranolol (4 × 10−6 m) enhanced the amplitude of e.j.p. generated by excitation of cholinergic nerves when repetitive stimulation (10 stimuli at 20 Hz) was used, but not the amplitude of the e.j.p. evoked by a single stimulus. 5‐Hydroxytryptamine (6 × 10−6 m) produced a tonic contracture of the dog trachea. After pretreatment with atropine (4 × 10−6 m), field stimulation (50 μs in duration and repetitive stimuli at 20 Hz) induced reversal of the contracture induced by 5‐hydroxytryptamine and this was abolished by propranolol (5 × 10−6 m). These results indicate that endogenous or exogenous catecholamines, in relatively low concentrations, predominantly activate β‐adrenoceptors in the pre‐ and post‐junctional membrane in the dog trachea, and induce muscle relaxation.

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SUMMARYEffects of morphine on the neuro-effector junction of the guinea-pig ileum or mouse vas deferens were investigated by the micro-electrode and double sucrose gap methods.