The physiology of the biliary tree. Motility of the gallbladder - Part 1
An incomplete picture has emerged of the complex means by which gallbladder motility is controlled under normal and pathophysiological conditions. In the first part of this review an overall account is presented. The mechanisms of cholecystokinin release, its stimulation by dietary factors and pepti...
Main Authors: | , |
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Format: | Article |
Language: | English |
Published: |
Wolters Kluwer Medknow Publications
1999-01-01
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Series: | The Saudi Journal of Gastroenterology |
Online Access: | http://www.saudijgastro.com/article.asp?issn=1319-3767;year=1999;volume=5;issue=3;spage=93;epage=105;aulast=Ballal |
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author | Ballal Mansour Sanford Paul |
author_facet | Ballal Mansour Sanford Paul |
author_sort | Ballal Mansour |
collection | DOAJ |
description | An incomplete picture has emerged of the complex means by which gallbladder motility is controlled under normal and pathophysiological conditions. In the first part of this review an overall account is presented. The mechanisms of cholecystokinin release, its stimulation by dietary factors and peptides elaborated by both pancreas and small intestine are discussed. The inhibition of cholecystokinin release by bile acids and proteases is also described. In the second part attention is focussed on other peptides affecting motility. These include (a) octreotide, effective for treatment of acromegaly, (b) peptide YY, contributing to a "colonic brake′, (c) motilin. associated with interdigestive contractions, analogues of which possibly correct gallbladder hypomotility, and (d) substance P and calcitonin gene-related peptide, which facilitate ganglionic transmission after release from extrinsic sensory neurones and alter gallbladder responses to vagal stimulation. The sympathetic nervous system and diabetes mellitus also influence vagal responses. The former, acting presynaptically, may provide a "brake" to prevent vagal overactivity. The latter could cause hypomotility via autonomic neuropathy, although hyperglycaemia, itself, may play a role. The role of nitric oxide, released from neurones also producing vasoactive intestinal peptide is recognized. Both lengthen muscle, the former producing responses without requiring plasma membrane receptors. Gallbladder motility also changes during pregnancy and stone formation. Progesterone and cholesterol can limit G protein actions, thus impairing contractions. Inflammation is associated with abnormal motility. The production of reactive oxygen metabolites, acting directly or releasing prokinetic prostaglandins, may be responsible. It has been proposed that the gastrointestinal tract may be normally in a state of controlled inflammation, primed to react to harmful challenges. |
first_indexed | 2024-04-13T01:28:14Z |
format | Article |
id | doaj.art-f74d0661e7c746dab2412e11236e005c |
institution | Directory Open Access Journal |
issn | 1319-3767 |
language | English |
last_indexed | 2024-04-13T01:28:14Z |
publishDate | 1999-01-01 |
publisher | Wolters Kluwer Medknow Publications |
record_format | Article |
series | The Saudi Journal of Gastroenterology |
spelling | doaj.art-f74d0661e7c746dab2412e11236e005c2022-12-22T03:08:35ZengWolters Kluwer Medknow PublicationsThe Saudi Journal of Gastroenterology1319-37671999-01-015393105The physiology of the biliary tree. Motility of the gallbladder - Part 1Ballal MansourSanford PaulAn incomplete picture has emerged of the complex means by which gallbladder motility is controlled under normal and pathophysiological conditions. In the first part of this review an overall account is presented. The mechanisms of cholecystokinin release, its stimulation by dietary factors and peptides elaborated by both pancreas and small intestine are discussed. The inhibition of cholecystokinin release by bile acids and proteases is also described. In the second part attention is focussed on other peptides affecting motility. These include (a) octreotide, effective for treatment of acromegaly, (b) peptide YY, contributing to a "colonic brake′, (c) motilin. associated with interdigestive contractions, analogues of which possibly correct gallbladder hypomotility, and (d) substance P and calcitonin gene-related peptide, which facilitate ganglionic transmission after release from extrinsic sensory neurones and alter gallbladder responses to vagal stimulation. The sympathetic nervous system and diabetes mellitus also influence vagal responses. The former, acting presynaptically, may provide a "brake" to prevent vagal overactivity. The latter could cause hypomotility via autonomic neuropathy, although hyperglycaemia, itself, may play a role. The role of nitric oxide, released from neurones also producing vasoactive intestinal peptide is recognized. Both lengthen muscle, the former producing responses without requiring plasma membrane receptors. Gallbladder motility also changes during pregnancy and stone formation. Progesterone and cholesterol can limit G protein actions, thus impairing contractions. Inflammation is associated with abnormal motility. The production of reactive oxygen metabolites, acting directly or releasing prokinetic prostaglandins, may be responsible. It has been proposed that the gastrointestinal tract may be normally in a state of controlled inflammation, primed to react to harmful challenges.http://www.saudijgastro.com/article.asp?issn=1319-3767;year=1999;volume=5;issue=3;spage=93;epage=105;aulast=Ballal |
spellingShingle | Ballal Mansour Sanford Paul The physiology of the biliary tree. Motility of the gallbladder - Part 1 The Saudi Journal of Gastroenterology |
title | The physiology of the biliary tree. Motility of the gallbladder - Part 1 |
title_full | The physiology of the biliary tree. Motility of the gallbladder - Part 1 |
title_fullStr | The physiology of the biliary tree. Motility of the gallbladder - Part 1 |
title_full_unstemmed | The physiology of the biliary tree. Motility of the gallbladder - Part 1 |
title_short | The physiology of the biliary tree. Motility of the gallbladder - Part 1 |
title_sort | physiology of the biliary tree motility of the gallbladder part 1 |
url | http://www.saudijgastro.com/article.asp?issn=1319-3767;year=1999;volume=5;issue=3;spage=93;epage=105;aulast=Ballal |
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