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Hormonal control of gastrointestinal motility

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Abstract

The objective of these studies was to assess the role of gastrointestinal hormones in controlling gastrointestinal motility. In the proximal stomach, cholecystokinin (CCK), gastrin, and secretin inhibit contractions, thereby decreasing intragastric pressure and slowing gastric emptying of liquids. Gastric inhibitory polypeptide (GIP), glucagon, and vasoactive intestinal peptide (VIP) may also slow gastric emptying, since they also inhibit proximal gastric contractions, but this was not tested. In contrast, motilin augments proximal gastric contractions and speeds gastric emptying of liquids. The contractions of the distal stomach are stimulated by gastrin, CCK, and motilin and inhibited by secretin, gastric inhibitory polypeptide, and VIP. The modulation of distal gastric contractions by these hormones may influence gastric trituration and emptying of solids, but this is unknown. Pyloric contractions are enhanced by CCK and secretin, an effect blocked by gastrin. Such enhancement ought to decrease duodenal-gastric reflux, but again, this is untested. In the small bowel, CCK, gastrin, motilin, VIP, and glucagon stimulate contractions, while secretin inhibits contractions. CCK and motilin speed small bowel transit, but VIP and glucagon slow transit. The cyclical bursts of gastroduodenal contractions that occur during fasting are associated with increased concentrations of motilin in the plasma, whereas the contractions characteristic of the fed state are copied by exogenous administration of gastrin and CCK. Of all these actions, only those of CCK on the proximal stomach, and gastrin on the distal stomach, have been shown to be physiologic so far.

Résumé

L'objet de ce travail est de préciser le rôle des hormones gastro-intestinales dans le contrôle de la motilité digestive. Au niveau de l'estomac proximal, la cholécystokinine (CCK), la gastrine et la sécrétine inhibent les contractions. Elles diminuent la pression intragastrique et ralentissent l'évacuation gastrique des liquides. Le polypeptide inhibiteur gastrique (GIP), le glucagon et le polypeptide intestinal vasoactif (VIP) ralentissent peutêtre aussi la vidange gastrique, car ils inhibent également les contractions gastriques proximales; mais cet effet sur la vidange n'a pas été étudié. A l'opposé, la motiline augmente les contractions de l'estomac proximal et accélère l'évacuation gastrique de liquides. Les contractions de l'estomac distal sont stimulées par la gastrine, la CCK et la motiline; elles sont inhibées par la sécrétine, le GIP et le VIP. Il est possible que la modulation des contractions gastriques par ces hormones influence le brassage intragastrique des aliments et l'évacuation des solides; mais ceci n'a pas été étudié. Les contractions du pylore sont accrues par la CCK et la sécrétine, et cet effet stimulant est bloqué par la gastrine. Cette stimulation devrait, en principe, réduire le reflux duodéno-gastrique; mais ceci n'a pas non plus été démontré. Au niveau de l'intestin grêle, la CCK, la gastrine, la motiline, le VIP et le glucagon stimulent les contractions, qui sont inhibées par la sécrétine. La CCK et la motiline accélèrent le transit intestinal; le VIP et le glucagon le ralentissent. Les bouffées cycliques de contractions gastroduodénales qui surviennent dans l'état de jeûne sont associées a une élévation des concentrations plasmatiques de motiline; les contractions caractéristiques de l'état postprandial sont reproduites par l'administration de gastrine et de CCK. A ce jour, la participation de ces effets hormonaux dans les mécanismes physiologiques n'a été démontrée que pour la CCK sur l'estomac proximal et pour la gastrine sur l'estomac distal.

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  1. Department of Surgery, Mayo Medical School, 55901, Rochester, Minnesota, USA

    Paul A. Thomas F.R.C.S., Onye E. Akwari M.D. & Keith A. Kelly M.D.

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Supported by USPHS NIH Grant AM18278, the Mayo Foundation and the Wellcome Trust.

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Thomas, P.A., Akwari, O.E. & Kelly, K.A. Hormonal control of gastrointestinal motility. World J. Surg. 3, 545–552 (1979). https://doi.org/10.1007/BF01654757

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