Nervous control of the internal anal sphincter of the cat.

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Abstract
The effects of sympathetic and parasympathetic efferent nerve stimulation on the activity of longitudinal and circular coats of the anal sphincteric area was studied on acute animals using extracellular electrical recordings. The effect of intramural sympathetic nerve stimulation was investigated on anal sphincteric circular muscle, with the sucrose gap technique. Hypogastric nerve stimulation elicited in anal sphincteric circular muscle slow time course depolarization responses (latency 200-400 ms) which were abolished by .alpha.-adrenergic blockers (dihydroergotamine, phentolamine). Stimulation of the parasympathetic outflow to the internal anal sphincter (2nd ventral sacral root: VS2) inhibited spontaneous electrical activity of the circular muscle. Pharmacological arguments lead to the conclusion that the inhibition induced by VS2 stimulation is mediated through intramural non-adrenergic non-cholinergic (purinergic) inhibitory neurons. Rectal distension caused an inhibition of the anal sphincteric circular muscle activity which persisted in the presence of atropine, phentolamine and propranolol, indicating that this inhibition was produced by non-adrenergic non-cholinergic intramural neurons. VS2 stimulation produced only an activation of the longitudinal muscle of the sphincteric area, which was abolished by hexamethonium and atropine; in contrast, hypogastric nerve stimulation gave rise to an inhibition which was blocked by propranolol. The longitudinal muscle receives an excitatory innervation from preganglionic parasympathetic nerves connected with intramural cholinergic neurons, and an inhibitory sympathetic innervation from noradrenergic axons running in the hypogastric nerves. No inhibitory non-adrenergic non-cholinergic innervation was observed in the longitudinal muscle in response to VS2 stimulation. Simultaneous stimulation of VS2 and hypogastric nerves indicate that in the anal sphincteric circular muscle the release of noradrenaline [norepinephrine] from sympathetic nerves is modulated by cholinergic receptors located on noradrenergic nerve endings, muscarinic receptors which can abolish the release of noradrenaline, and probably nicotinic receptors which increase the noradrenaline release. The eventual functional significance of the nicotinic receptors is discussed.