Abstract
Cholecystokinin (CCK) stimulates vagal afferent fiber discharge, both gastric and intestinal, which seems to result in reflex decrease in gastric motility, gastric acid secretion, and stimulation of pancreatic protein secretion. Endogenous release of CCK by fat or soybean trypsin inhibitor also alters function by way of a capsaicin-sensitive pathway. We suggest that CCK is released locally from the intestine and acts locally or systemically to stimulate vagal afferent fiber discharge to alter proximal gastrointestinal function (Fig. 14). In this way, in addition to its effect on food intake, CCK and the neural pathway integrate function in the proximal gastrointestinal tract, regulating the entry of food into the duodenum to ensure effective digestion and absorption.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Afferent Pathways / drug effects
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Afferent Pathways / physiology
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Animals
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Benzodiazepinones / pharmacology
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Cholecystokinin / pharmacology*
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Cholecystokinin / physiology*
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Devazepide
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Eating / drug effects
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Eating / physiology*
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Gastric Emptying / drug effects
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Mechanoreceptors / drug effects
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Mechanoreceptors / physiology
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Nerve Endings / drug effects
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Nerve Endings / physiology
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Rats
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Receptors, Cholecystokinin / antagonists & inhibitors
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Receptors, Cholecystokinin / physiology
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Sincalide / pharmacology
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Stomach / drug effects
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Stomach / innervation
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Stomach / physiology*
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Vagus Nerve / drug effects
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Vagus Nerve / physiology*
Substances
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Benzodiazepinones
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Receptors, Cholecystokinin
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Cholecystokinin
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Devazepide
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Sincalide