Abstract
The smooth muscle relaxant effects of dopamine observed in vascular tissue also extend to the smooth muscle of the gastrointestinal tract. For example, dopamine is known to relax the lower esophageal sphincter and has been suggested as a mediator of receptive relaxation of the stomach (Valenzuela, 1976). In contrast, contraction of GI muscle to dopamine has been reported from several locations in the GI tract in at least two species (Lanfranchi et al., 1978a; Anuras, 1981). Besides these smooth muscle effects, dopamine has a number of other interesting effects on GI function. Dopamine reduces pentagastrin-stimulated acid secretion in man, and it has been implicated in animal experiments to be involved in the pathogenesis of duodenal ulcer disease (Szabo, 1979). In fact, dopamine agonists may be antiulcerogenic drugs. A dopaminergic effect on electrolyte absorption has been demonstrated for the rabbit ileum. An additional effect of dopamine on GI function is its ability to increase blood flow through the arteries supplying most of the stomach and small intestine. Whether some or all of these GI effects of dopamine are physiologically relevant, especially in man, is still very much open to question. The presence of gut dopamine receptors appears to vary not only among species but among organs of the GI tract within one species. A thorough characterization of these receptors has not been performed. The evidence to date will be presented in the text of this chapter.
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Ormsbee, H.S. (1984). Dopamine Agonists/Antagonists in the Treatment of Gastrointestinal Diseases. In: Poste, G., Crooke, S.T. (eds) Dopamine Receptor Agonists. New Horizons in Therapeutics. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0310-8_16
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