Smooth muscle function and dysfunction in gallbladder disease

被引:62
作者
Portincasa P. [1 ]
Di Ciaula A. [1 ]
vanBerge-Henegouwen G.P. [2 ]
机构
[1] Section of Internal Medicine, Dept. of Internal Med./Public Health, University Medical School, 70124 Bari
[2] Gastrointestinal Research Unit, University of Medical Center, Utrecht
关键词
Cholesterol Gallstone; Human Gallbladder; Physiol Gastrointest Liver; Gallbladder Contraction; Gallstone Patient;
D O I
10.1007/s11894-004-0043-0
中图分类号
学科分类号
摘要
The gallbladder epithelium and smooth muscle layer are exposed to concentrated biliary solutes, including cholesterol and potentially toxic hydrophobic bile salts, which are able to influence muscle contraction. Physiologically, gallbladder-tone is regulated by spontaneous muscle activity, hormones, and neurotransmitters released into the muscle from intrinsic neurons and extrinsic sympathetic nerves. Methods to explore gallbladder smooth muscle function in vitro include cholecystokinin (CCK) receptor-binding studies and contractility studies. In human and animal models, studies have focused on cellular and molecular events in health and disease, and in vitro findings mirror in vivo events. The interplay between contraction and relaxation of the gallbladder muscularis leads in vivo to appropriate gallbladder emptying and refilling during fasting and postprandially. Defective smooth muscle contractility and/or relaxation are found in cholesterol stone-containing gallbladders, featuring a type of gallbladder leiomyopathy; defects of CCKA receptors and signal transduction may coexist with abnormal responses to oxidative stress and inflammatory mediators. Abnormal smooth musculature contractility, impaired gallbladder motility, and increased stasis are key factors in the pathogenesis of cholesterol gallstones. Copyright © 2004 by Current Science Inc.
引用
收藏
页码:151 / 162
页数:11
相关论文
共 133 条
  • [31] Aoki T., Ueno T., Toyonaga A., Et al., Radiographic evidence of cholecystokinin octapeptide receptors in the hamster gallbladder, Scand. J. Gastroenterol., 26, pp. 1165-1172, (1991)
  • [32] Bitar K.N., Bradford P.G., Putney J.W., Makhlouf G.M., Stoichiometry of contraction and Ca2+ mobilization by inositol-1,4,5-trisphosphate in isolated gastric smooth muscle cells, J. Biol. Chem., 261, pp. 16591-16596, (1986)
  • [33] Chen Q., Yu P., De Petris G., Et al., Distinct muscarinic receptors and signal transduction pathways in gallbladder muscle, J. Pharmacol. Exp. Ther., 273, pp. 650-655, (1995)
  • [34] Yu P., Chen Q., Harnett K.M., Et al., Direct G protein activation reverses impaired CCK signaling in human gallbladders with cholesterol stones, Am. J. Physiol., 269, (1995)
  • [35] Chen Q., De Petris G., Yu P., Et al., Different pathways mediate cholecystokinin actions in cholelithiasis, Am. J. Physiol., 272, (1997)
  • [36] Yu P., Chen Q., Biancani P., Behar J., Membrane cholesterol alters gallbladder muscle contractility in prairie dogs, Am. J. Physiol., 271, (1996)
  • [37] Amaral J., Xiao Z.L., Chen Q., Et al., Gallbladder muscle dysfunction in patients with chronic acalculous disease, Gastroenterology, 120, pp. 506-511, (2001)
  • [38] Portincasa P., Di Ciaula A., Baldassarre G., Et al., Gallbladder motor function in gallstone patients: Sonographic and in vitro studies on the role of gallstones, smooth muscle function and gallbladder wall inflammation, J. Hepatol., 21, pp. 430-440, (1994)
  • [39] Bird N.C., Wegstapel H., Chess-Williams R., Johnson A.G., In vitro contractility of stimulated and non-stimulated human gallbladder muscle, Neurogastroenterol. Motil., 8, pp. 63-68, (1996)
  • [40] Severi C., Grider J.R., Makhlouf G.M., Functional gradients in muscle cells isolated from gallbladder, cystic duct, and common bile duct, Am. J. Physiol., 255, (1988)