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Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors.
Gastroenterology. 1998 Sep; 115(3):597-604.G

Abstract

BACKGROUND & AIMS

Exogenous cholecystokinin (CCK) decreases lower esophageal sphincter (LES) pressure and increases transient LES relaxations (TLESRs) in humans. The aims of this study were to determine whether endogenous CCK increases gastroesophageal reflux in humans and whether this is a direct effect on the LES.

METHODS

Esophageal pH, LES pressure, and gallbladder volume were measured in 8 healthy volunteers after ingestion of a 181-kcal meal alone or adding 12 g cholestyramine to increase endogenous CCK release. In 7 additional volunteers, the effect of cholestyramine was studied during intravenous perfusion of saline or the CCK-A receptor antagonist loxiglumide. In circular LES strips from 9 transplant donors, we measured the effect of CCK-8 (10(-11) to 3 x 10(-8) mol/L) on basal tension and on electrical field-induced relaxation.

RESULTS

Cholestyramine increased gallbladder emptying, reflux episodes, TLESRs, and time of esophageal pH of <4. Loxiglumide inhibited postprandial gallbladder emptying, reflux episodes, TLESRs, and time of pH of <4 and prevented the decrease in LES pressure induced by cholestyramine. In vitro, CCK-8 contracted LES strips through a tetrodotoxin-insensitive pathway but did not modify electrical field-induced LES relaxations.

CONCLUSIONS

Endogenous CCK enhances postprandial gastroesophageal reflux in humans by increasing the rate of TLESRs and reduces postprandial LES pressure. These actions seem mediated by extrasphincteric CCK-A receptors that override a direct contractile effect of CCK on the LES muscle.

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Authors+Show Affiliations

Clavé P
Laboratori d'Investigació Gastrointestinal, Institut de Recerca, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
González A
No affiliation info available
Moreno A
No affiliation info available
López R
No affiliation info available
Farré A
No affiliation info available
Cussó X
No affiliation info available
D'Amato M
No affiliation info available
Azpiroz F
No affiliation info available
Lluís F
No affiliation info available

MeSH

AdultCholecystokininCholestyramine ResinEatingElectric StimulationEsophagogastric JunctionEsophagusGallbladderGastroesophageal RefluxHumansHydrogen-Ion ConcentrationIn Vitro TechniquesMaleMuscle ContractionMuscle RelaxationMuscle, SmoothProglumideReceptor, Cholecystokinin AReceptors, CholecystokininSincalide

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9721157

Citation

Clavé, P, et al. "Endogenous Cholecystokinin Enhances Postprandial Gastroesophageal Reflux in Humans Through Extrasphincteric Receptors." Gastroenterology, vol. 115, no. 3, 1998, pp. 597-604.
Clavé P, González A, Moreno A, et al. Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors. Gastroenterology. 1998;115(3):597-604.
Clavé, P., González, A., Moreno, A., López, R., Farré, A., Cussó, X., D'Amato, M., Azpiroz, F., & Lluís, F. (1998). Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors. Gastroenterology, 115(3), 597-604.
Clavé P, et al. Endogenous Cholecystokinin Enhances Postprandial Gastroesophageal Reflux in Humans Through Extrasphincteric Receptors. Gastroenterology. 1998;115(3):597-604. PubMed PMID: 9721157.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors. AU - Clavé,P, AU - González,A, AU - Moreno,A, AU - López,R, AU - Farré,A, AU - Cussó,X, AU - D'Amato,M, AU - Azpiroz,F, AU - Lluís,F, PY - 1998/8/28/pubmed PY - 1998/8/28/medline PY - 1998/8/28/entrez SP - 597 EP - 604 JF - Gastroenterology JO - Gastroenterology VL - 115 IS - 3 N2 - BACKGROUND & AIMS: Exogenous cholecystokinin (CCK) decreases lower esophageal sphincter (LES) pressure and increases transient LES relaxations (TLESRs) in humans. The aims of this study were to determine whether endogenous CCK increases gastroesophageal reflux in humans and whether this is a direct effect on the LES. METHODS: Esophageal pH, LES pressure, and gallbladder volume were measured in 8 healthy volunteers after ingestion of a 181-kcal meal alone or adding 12 g cholestyramine to increase endogenous CCK release. In 7 additional volunteers, the effect of cholestyramine was studied during intravenous perfusion of saline or the CCK-A receptor antagonist loxiglumide. In circular LES strips from 9 transplant donors, we measured the effect of CCK-8 (10(-11) to 3 x 10(-8) mol/L) on basal tension and on electrical field-induced relaxation. RESULTS: Cholestyramine increased gallbladder emptying, reflux episodes, TLESRs, and time of esophageal pH of <4. Loxiglumide inhibited postprandial gallbladder emptying, reflux episodes, TLESRs, and time of pH of <4 and prevented the decrease in LES pressure induced by cholestyramine. In vitro, CCK-8 contracted LES strips through a tetrodotoxin-insensitive pathway but did not modify electrical field-induced LES relaxations. CONCLUSIONS: Endogenous CCK enhances postprandial gastroesophageal reflux in humans by increasing the rate of TLESRs and reduces postprandial LES pressure. These actions seem mediated by extrasphincteric CCK-A receptors that override a direct contractile effect of CCK on the LES muscle. SN - 0016-5085 UR - https://www.unboundmedicine.com/medline/citation/9721157/Endogenous_cholecystokinin_enhances_postprandial_gastroesophageal_reflux_in_humans_through_extrasphincteric_receptors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0016508598002443 DB - PRIME DP - Unbound Medicine ER -