Abstract
The gastrointestinal polypeptide gastrin, found in great abundance in the gastric antrium, was shown in 1970 to have a very dramatic effect in stimulating the smooth muscle segment of the lower esophageal sphincter (LES), and in causing marked increases in pressure in this region. 1 This observation resulted in numerous studies confirming this effect, and led to the suggestion that endogenous gastrin might be a major controlling factor in setting the level of pressure in the LES and, in fact, that gastrin might be the major determinant of LES pressure. 2 More recently, there has been considerable controversy related to the possibility that some of these sphincteric effects of gastrin (or pentagastin) might be more in the order of pharmacologic responses due to large doses of exogenous gastrin, and raising serious questions as to the specific physiologic role of endogenous gastrin in maintenance of LES pressure. There are a number
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