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The anal sphincter is a complex anatomical structure consisting of the internal anal sphincter (IAS), an involuntary smooth muscle, and the external anal sphincter (EAS), a voluntary skeletal muscle (StatPearls, 2023). Its primary biological function is the maintenance of fecal continence and the regulation of defecation through coordinated contraction and relaxation (NIH, 2022). Dysfunction of the anal sphincter is central to several proctological disorders; for example, hypertonicity of the IAS is associated with chronic anal fissures and impaired mucosal blood flow, while sphincter insufficiency leads to fecal incontinence (Mayo Clinic, 2023). While the anal sphincter itself is an anatomical structure rather than a single molecular target, it contains various receptors and ion channels that are targeted by drugs. Topical nitrates (e.g., nitroglycerin) act as nitric oxide donors to relax the IAS, and calcium channel blockers (e.g., diltiazem) are used to reduce resting pressure by inhibiting smooth muscle contraction (PubMed, 2021). Additionally, botulinum toxin is used to induce temporary muscle paralysis by inhibiting acetylcholine release at the neuromuscular junction (ASGE, 2020). Therapeutic interventions aim to restore normal pressure and function to alleviate symptoms and promote tissue healing.
Pharmacological agents target the anal sphincter by modulating smooth muscle tone through nitric oxide donation, calcium channel blockade, or inhibition of neurotransmitter release at the neuromuscular junction.
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