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The external anal sphincter is the ring of skeletal muscle surrounding the distal anal canal. Its contraction helps maintain faecal continence; its motor neurons allow voluntary squeezing as well as reflex control. It works alongside the smooth muscle of the internal anal sphincter, so continence depends on coordinated structures rather than one isolated ring.^[ref]

Branches of the pudendal nerve supply the external anal sphincter. Dissection of 28 cadavers found a local nerve plexus near the sphincters in five, illustrating why a schematic nerve route need not capture every individual's branching. Preserving muscle alone therefore does not guarantee preservation of its motor supply.^[ref]

The internal anal sphincter is a ring of smooth muscle at the lower end of the rectum and around the upper anal canal. It contributes involuntary resting closure. The surrounding external anal sphincter is a different muscle system with voluntary control, so the two should not be treated as one anatomical ring.^[ref]

Rectal distension can trigger relaxation of the internal anal sphincter, the rectoanal inhibitory reflex. Researchers can inflate a rectal balloon while recording anal pressure, separating this relaxation from other contractile responses and from reported sensation. A study of 23 subjects observed inhibitory and contractile reflexes during graded balloon distension.^[ref] A continuous pressure trace therefore reveals coordinated components of continence that are difficult to infer from static anatomy alone.

The rectoanal inhibitory reflex is relaxation of the internal anal sphincter in response to distension of the rectum. Because the internal anal sphincter is smooth muscle, this relaxation is distinct from voluntary control of the external anal sphincter. In manometry, a rectal balloon supplies a controlled distension while anal pressure sensors record the response over time.^[ref]

A fall in pressure can coexist with a contractile response elsewhere or at another time. The same study measured inhibitory and contractile reflexes and asked subjects about sensation; a relaxation trace therefore cannot simply be equated with the conscious urge to empty the rectum.^[ref]

A complementary experiment recorded tension in isolated human internal anal sphincter strips. A donor of nitric oxide relaxed the strips; blocking its synthesis suppressed relaxation evoked by electrical nerve stimulation, and arginine reversed the inhibition in a stereospecific control. These interventions support a role for nitric oxide in nerve-mediated relaxation. An isolated strip identifies a mechanism in the effector muscle; it does not reproduce the whole intact reflex circuit.^[ref]

T. O'Kelly is the first author of a 1993 study testing the role of nitric oxide in relaxation of the human internal anal sphincter. Isolated muscle strips were mounted in organ baths for measurement of tension at fixed length. Electrical stimulation evoked nerve-dependent relaxation, allowing the investigators to test which chemical pathway connected stimulation to the mechanical response.^[ref]

Several interventions converged on the same explanation. A compound releasing nitric oxide relaxed the strips; inhibitors of nitric oxide synthase suppressed electrically evoked relaxation; adding the appropriate form of arginine reversed that inhibition. The opposite enantiomer did not have the same effect. A substance that scavenges nitric oxide also abolished the response. This combination of mimicry, inhibition, rescue and specificity controls supported a role for nitric oxide in neural relaxation of smooth muscle. It provided stronger causal evidence than observing a correlation between chemical abundance and relaxation alone.^[ref]