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...

Full description

Bibliographic Details
Main Authors: Ballal Mansour, Sanford Paul
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 1999-01-01
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
_version_ 1811281138499452928
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
work_keys_str_mv AT ballalmansour thephysiologyofthebiliarytreemotilityofthegallbladderpart1
AT sanfordpaul thephysiologyofthebiliarytreemotilityofthegallbladderpart1
AT ballalmansour physiologyofthebiliarytreemotilityofthegallbladderpart1
AT sanfordpaul physiologyofthebiliarytreemotilityofthegallbladderpart1