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The Sphincter of Oddi is a specialized smooth muscle valve located at the junction of the common bile duct, the pancreatic duct, and the second part of the duodenum [6, 8]. Its primary physiological role is to regulate the intermittent flow of bile and pancreatic enzymes into the small intestine while preventing the retrograde reflux of duodenal contents, which protects the biliary tree from infection and sludge accumulation [1, 2, 8]. The sphincter is under complex neurohumoral control, primarily regulated by the hormone cholecystokinin (CCK), which promotes relaxation to facilitate digestion [1, 7, 10]. Clinical dysfunction of this structure, termed Sphincter of Oddi Dysfunction (SOD), often manifests as severe biliary pain or recurrent pancreatitis, particularly in post-cholecystectomy patients [4, 9, 13]. Pharmacologically, the sphincter is a site of significant drug-tissue interaction; for example, opioid analgesics can induce paradoxical spasms and increase biliary pressure, whereas nitrates and calcium channel blockers are used to promote relaxation and alleviate symptoms [2, 3, 12]. Understanding the pharmacological response of this sphincter is essential for managing gastrointestinal disorders and ensuring safety during endoscopic retrograde cholangiopancreatography (ERCP) [11, 13].
Drugs modulate the Sphincter of Oddi by acting on various G protein-coupled receptors (e.g., mu-opioid, CCK1, and muscarinic receptors) or by directly affecting smooth muscle contraction through calcium channel inhibition or nitric oxide-mediated vasodilation [2, 3, 8, 11, 12].
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