title: The internal anal sphincter: mechanisms of control and its role in maintaining anal continence.
abstract: The human IAS has particular structural and functional characteristics. This smooth muscle constantly generates rhythmic electrical slow waves, but no action potentials. The slow waves are linked to calcium fluxes and both are essential for mechanical activity, i.e. the ASPW. The IAS is pharmacologically characterized by the presence of alpha excitatory and beta inhibitory adrenergic receptors. Cholinergic drugs have an indirect effect through the release of an inhibitory neurotransmitter, very probably VIP, from NANC nerves. The myogenic activity of the IAS is enhanced by its extrinsic sympathetic innervation. Thus, at rest, the IAS is in a state of partial tetanus and contributes approximately 55% of the MABP. Because the IAS ring cannot be completely closed, the anal mucosa and the haemorrhoidal plexuses fill the gap. By compressing these tissues, the IAS perfectly closes the anal canal to retain not only solids but also fluid stool and gas. Acute rectal distension and rectal activity, mainly through intramural pathways, induce reflex IAS relaxation, permitting the rectal contents to be sampled by receptors in the upper anal canal while continence is temporarily maintained by EAS activity and by expansion of the haemorrhoidal cushions. There is a correlation between the volume of rectal distension and the parameters of IAS relaxation. At maximal IAS relaxation, ASPW are absent, indicating the completeness of the inhibition. Although this RAIR is not essential for defecation, insufficient relaxation may be implicated in constipation. Hyperactivity of the IAS resulting in a high MABP and AUSPW has been considered both as a cause and as an effect in haemorrhoids and anal fissure. Continence for fluids and gas is impaired if IAS activity is decreased (i.e. a low MABP), either by direct trauma or by damage of its sympathetic innervation. Severe faecal incontinence will develop when the contractility of both the IAS and the EAS is affected.
authors.forename: F
authors.initials: F
authors.lastname: Penninckx
authors.forename: B
authors.initials: B
authors.lastname: Lestar
authors.forename: R
authors.initials: R
authors.lastname: Kerremans
mesh_terms: D001003:Anal Canal / Q000502:physiology*; D001004:Anus Diseases / Q000503:physiopathology; D003672:Defecation / Q000502:physiology*; D004594:Electrophysiology; D005242:Fecal Incontinence / Q000503:physiopathology; D005769:Gastrointestinal Motility / Q000502:physiology; D006801:Humans; D012002:Rectal Diseases / Q000503:physiopathology; D012018:Reflex / Q000502:physiology