SUMMARY1. Responses ofthe smooth muscle membrane ofthe rabbit bladder to intramuscular nerve stimulation were investigated by the micro-electrode and double sucrose-gap methods.2. The cell generated regular spontaneous action potentials. Acetylcholine produced a maintained increase in the frequency and ATP a transient increase. Noradrenaline only increased the frequency at very high concentrations.3. Application of short current pulses (50/isec) produced an initial excitatory junction potential (e.j.p.) with a superimposed spike, followed by a late depolarization. On some occasions, hyperpolarization of the membrane appeared between initial e.j.p. and the late depolarization. All these responses were abolished by tetrodotoxin.4. The late depolarization was enhanced by pre-treatment with neostigmine and abolished by atropine. This means that the delayed depolarization is due to activation ofthe muscarinic receptor. When the late depolarization was abolished, the amplitude of hyperpolarization was enhanced.5. The e.j.p. and contraction were unaffected by guanethidine, phentolamine, methysergide, mepyramine, quinidine or theophylline. This means that the e.j.p. is not mediated by activation of adrenergic, tryptaminergic, histaminergic or purinergic receptors.6. ATP reduced the amplitude of the e.j.p. due to depolarization of the membrane and reduction in the membrane resistance. The amplitude of the e.j.p. was gradually reduced by repetitive stimulation (0-5-2-0 Hz). However, the rate of depression was unchanged in the presence of ATP. Dipyridamole did not change the electrical and mechanical responses to field stimulation. These results do not support the proposal that ATP is the non-cholinergic excitatory transmitter.7. Apamine and tetraethylammonium (TEA) suppressed the hyperpolarization produced by field stimulation but guanethidine did not inhibit the hyperpolarization. Therefore, the hyperpolarization is due to increased K conductance of the membrane but it is not possible to conclude whether this component is due to the inhibitory action of a neurotransmitter or solely to after hyperpolarization of the spike.8. It was concluded that the rabbit bladder receives both cholinergic and noncholinergic excitatory neurones.

No abstract

1 Strips of urethra taken from guinea-pigs contracted in response to acetylcholine, noradrenaline (via a-adrenoceptors) and 5-hydroxytryptamine, and were relaxed by adenosine triphosphate (ATP) if the tone was raised. Isoprenaline produced relaxation of bladder strips (via Padrenoceptors) whereas ATP caused contraction. 2 Atropine completely blocked all responses to acetylcholine; quinidine failed to block ATP responses selectively; methysergide blocked responses of the urethra but not the bladder to 5-hydroxytryptamine. 3 Spontaneous electrical activity was recorded with intracellular microelectrodes from all regions: in the urethra infrequent bursts of spikes occurred at 1-7 min intervals; regular spikes at 6-30/min were recorded from the detrusor muscle. In the bladder base, bursts of spikes were superimposed on the regular pattern. 4 Bursts of spikes in the urethra were initiated by noradrenaline, phenylephrine or acetylcholine and inhibited by ATP; regular spikes in the bladder were accelerated by acetylcholine or ATP and slowed by noradrenaline or isoprenaline. 5 The intrinsic electrical activity and pharmacological properties of the urethra therefore differ from those of the bladder. This may account for the different responses of the two regions in normal function.

1. In anaesthetized dogs, resting mean penile artery pressure (p.a.p.) and corpus cavernosum pressure (c.c.p.) were 70‐100% and 10‐15% of mean systemic blood pressure, respectively. 2. Stimulation of the pelvic nerve at 10 Hz produced an immediate drop in p.a.p. and c.c.p., followed 10‐30 s later by a rise in c.c.p. to the level of p.a.p. This level was 60‐90% of systemic pressure, and was maintained throughout stimulation. 3. The threshold for a rise in c.c.p. was 3‐5 Hz. Atropine (1 mg/kg), phentolamine (200 micrograms kg‐1) and propranolol (200 micrograms kg‐1) had no effect on the response to pelvic nerve stimulation. 4. C.c.p., p.a.p. and their changes in response to pelvic nerve stimulation were not significantly altered by either stimulation or section of the hypogastric nerves. 5. Cutting the sympathetic chain on both sides at L5, or administration of phentolamine, had no effect on resting c.c.p. or p.a.p. However, subsequent responses to pelvic nerve stimulation were enhanced. 6. When the pelvic nerve was stimulated during excitation of the sympathetic chain, there was still an initial drop in p.a.p. and c.c.p. but the subsequent increase in c.c.p. was delayed or abolished. These effects were mimicked by close arterial injection of phenylephrine and blocked by alpha‐adrenergic antagonists. 7. This study suggests that erections in response to pelvic nerve stimulation result from an initial increase in volume of the corpus spongiosum, followed 20 s later by a stiffening of the corpus cavernosum as its pressure increases. Only the latter process is inhibited by activity of the sympathetic fibres.