Nitric oxide, the nonandrenergic, noncholingergic neurotransmitter, appears to be the inhibitory neurotransmitter that effects lower esophageal sphincter relaxation. Perturbations in this neurotransmitter axis may be responsible for diseases associated with lower esophageal sphincter dysfunction leg, gastroesophageal reflux disease, achalasia). It is likely that efforts directed at correcting the perturbation in nitric oxide effect will result in novel treatments for these diseases. As increasing options for treatment of achalasia become available, the optimal approach to therapy may finally be realized. Appropriate economic models will need to be developed, because it is unlikely that long-term controlled clinical trials comparing surgical therapy with endoscopic or pharmacologic therapy will be performed. Finally, dysfunction of the upper esophageal sphincter is being increasingly recognized; however, appropriate evaluation, treatment, and natural history of these disorders are as yet unknown.
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