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Mechanism of the Lower Esophageal Sphincter Relaxation ACTION OF PROSTAGLANDIN E1 AND THEOPHYLLINE
Raj K. Goyal, Satish Rattan
Raj K. Goyal, Satish Rattan
Published February 1, 1973
Citation Information: J Clin Invest. 1973;52(2):337-341. https://doi.org/10.1172/JCI107189.
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Research Article

Mechanism of the Lower Esophageal Sphincter Relaxation ACTION OF PROSTAGLANDIN E1 AND THEOPHYLLINE

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Abstract

The intravenous injection of prostaglandin E1 (PGE1) causes a dose-dependent relaxation of the lower esophageal sphincter (LES) in the intact, lightly anesthetized opossum. The action of PGE1 is not inhibited by the drugs that produce muscarinic or nicotinic cholinergic antagonism or alpha and beta adrenergic antagonism in the doses that inhibited the action of respective agonists. Moreover, this action is not affected by exogenous gastrin pentapeptide. The action of PGE1 on the LES is mimicked by isoproterenol, theophylline ethylenediamine, and dibutyryl cyclic AMP. Both theophylline, a phosphodiesterase inhibitor, and isoproterenol, an adenyl cyclase stimulator, added to the action of PGE1. On the other hand, adenyl cyclase inhibitor nicotinic acid, as well as phosphodiesterase stimulator, imidazole inhibited its action. Further, both nicotinic acid and imidazole inhibited the degree of LES relaxation produced by esophageal distension. These studies suggest that intracellular cyclic AMP may act as the “second messenger” in the regulation of the lower esophageal sphincter relaxation.

Authors

Raj K. Goyal, Satish Rattan

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