Reassessing the role of nitric oxide in the pathogenesis of sphincter of Oddi dysfunction.

Abstract

The pathogenic mechanisms underlying sphincter of Oddi dysfunction (SOD) remain incompletely understood, and it often leads to severe symptoms encompassing nausea, vomiting, and abdominal pain. New evidence now suggests correlations between nitric oxide (NO) and SOD. In this review, we summarized the factors influencing SOD pathogenesis via NO and its derivative, the peroxynitrite anion. NO appears to enhance SOD progression by modulating sphincter of Oddi (SO) contractions via NO-sGC-cGMP signaling or inducing the apoptosis of enteric neurons, interstitial cells of Cajal, smooth muscle cells, and other cellular components via peroxynitrite anion-mediated organelle damage. Thus, a comprehensive understanding of SOD will provide a foundation for the identification of potential drugs and treatment approaches.