The sphincter of Oddi is a small sphincter which is strategically placed at the 
junction of the bile duct and pancreatic duct with the duodenum. It regulates 
the flow of bile and pancreatic juice into the duodenum and prevents reflux of 
duodenal contents into the ducts. The structure of the sphincter of Oddi differs 
from species to species and consequently its physiological action varies in 
different species. Anatomical and immunohistochemical investigations have 
demonstrated that the sphincter of Oddi is richly innervated by cholinergic, 
adrenergic and peptidergic neurons. In addition, neural connections exist 
between the sphincter, gallbladder and proximal gastrointestinal tract. These 
nerves in addition to hormones are important in the control of sphincter of Oddi 
motility and function. The normal human sphincter of Oddi is characterized by 
prominent phasic contractions which are superimposed on a modest basal pressure. 
These contractions are present throughout the interdigestive period. The 
contractions and basal pressure are inhibited by ingestion of a meal or infusion 
of cholecystokinin octapeptide, thus enhancing the flow of bile and pancreatic 
juice into the duodenum. Sphincter of Oddi dysfunction has been described in 
patients who present with recurrent biliary type pain and no evidence of a 
structural cause for the pain. Motility disorders characterized as an elevated 
basal pressure, rapid contraction frequency, paradoxical response to 
cholecystokinin octapeptide or excess of retrograde contractions have been 
identified. A number of pharmacologically active substances have been used in an 
attempt to treat these patients. Such pharmaceuticals include nitrites, Ca2+ 
channel blockers and smooth muscle relaxants. Their effect is transient and side 
effects relating to cardiovascular actions preclude their longterm use. Division 
of the sphincter either endoscopically or by open operation has been 
demonstrated by prospective clinical trials to be the most efficacious treatment 
for patients with a stenosed sphincter manometrically demonstrated by a high 
basal pressure. Improved understanding of the controlling mechanisms of 
sphincter of Oddi motility and the pathophysiology of sphincter of Oddi 
dysfunction should assist in the development of effective pharmacotherapy for 
these disorders.