Endothelin receptors in human and guinea-pig gallbladder muscle

Huang, Shih-Che; Lee, Ming-Che; Wei, Chang-Kao; Huang, Shih-Chang

doi:10.1016/s0167-0115(00)00238-x

Cited by 26 publications

(36 citation statements)

References 28 publications

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“…In contrast, ET B receptor had similar high affinities for ET-1, ET-2 and ET-3. ET B receptor, with a Bmax of 460 fmol/mg protein, was present 4 times in numbers to ET A receptor, with a Bmax of 110 fmol/mg protein [43] (Table 2).…”

Section: Guinea-pig Gallbladdermentioning

confidence: 99%

“…ET causes smooth muscle contraction through interaction with ET A receptors, ET B receptors or both subtypes, depending on tissues and species [5,[33][34][35][36][37][38][39][40][41][42][43][44]. Previous studies have shown that ET causes gastrointestinal muscle contraction through interaction with both ET A and ET B receptors in the esophageal muscularis mucosae, gallbladder, ileum and cecum [33,34,37,[40][41][42][43]. On the other hand, although the common bile duct muscle and gastric smooth muscle cells possess both ET A and ET B receptors, only ET A receptors mediate contraction [35,44].…”

Section: Endothelins and The Gastrointestinal Tractmentioning

confidence: 99%

“…In the hepatobiliary system, ET causes contraction of the portal vein, hepatic stellate cells, the gallbladder and common bile duct [41][42][43][44][71][72][73][74][75][76][77][78][79][80][81]. On the other hand, ET inhibits carbachol-induced contraction in the sphincter of Oddi [82] ( Table 3).…”

Section: Endothelins and The Hepatobiliary Systemmentioning

confidence: 99%

“…In the gastrointestinal system, ET causes smooth muscle contraction through interaction with ET A receptors, ET B receptors or both ET A and ET B receptors, dependent on tissue types and species. In addition to contraction, ET causes smooth muscle relaxation through interaction with ET A receptors or ET B receptors [32][33][34][35][36][37][38][39][40][41][42][43][44] (Fig. 3 Human ET-1…”

Section: Introductionmentioning

confidence: 99%

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Endothelin Receptors in Gastrointestinal Smooth Muscle

Huang

2005

CPPS

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Endothelins (ETs) are a family of peptides with 21-amino-acid residues. ET-1 was identified as a potent vasoconstrictor produced by vascular endothelial cells. Three distinct isoforms of ET, i.e. ET-1, ET-2 and ET-3, have been found to exist in a variety of tissues. ET was later found to cause contraction as well as relaxation of smooth muscle in many physiologic systems. In the gastrointestinal tract, ET causes contraction and/or relaxation of the esophagus, stomach, ileum and colon. In the hepatobiliary system, ET causes contraction of the portal vein, hepatic stellate cells, gallbladder and common bile duct. In mammalian species, two classes of ET receptors, ET(A) and ET(B), have been cloned. ET(A) receptors have higher affinities for ET-1 and ET-2 than ET-3, while ET(B) receptors have the same affinities for ET-1, ET-2 and ET-3. In the gastrointestinal system, ET causes smooth muscle contraction through interaction with ET(A) receptors, ET(B) receptors or both ET(A) and ET(B) receptors, depending on the tissues and species. In addition to contraction, ET causes smooth muscle relaxation through interaction with ET(A) receptors or ET(B) receptors. At the present time, there are no studies showing that ET causes smooth muscle relaxation through interaction with both ET(A) and ET(B) subtypes. ET induces contraction in most of the non-sphincter muscle except the fundus of the stomach. On the other hand, ET causes relaxation and contraction in the lower esophageal and internal anal sphincters. ET may play an important role in the control of human gastrointestinal motility and portal vein pressure.

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Section: Guinea-pig Gallbladdermentioning

confidence: 99%

Section: Endothelins and The Gastrointestinal Tractmentioning

confidence: 99%

Section: Endothelins and The Hepatobiliary Systemmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Endothelin Receptors in Gastrointestinal Smooth Muscle

Huang

2005

CPPS

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“…12,19•,23•,33,36,38•,51,59,61•,62-67,68•,70•,71•,[72][73][74][75][76][77][78][79][80][81][82]. Alternatively, whole gallbladders of the guinea pig or ground squirrel are studied by tensiometry[83][84][85].…”

mentioning

confidence: 99%

Smooth muscle function and dysfunction in gallbladder disease

Portincasa

Ciaula

vanBerge-Henegouwen³

2004

Curr Gastroenterol Rep

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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.

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Coordinate regulation of gallbladder motor function in the gut-liver axis

et al. 2008

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Gallstones are one of the most common digestive diseases with an estimated prevalence of 10%-15% in adults living in the western world, where cholesterol-enriched gallstones represent 75%-80% of all gallstones. In cholesterol gallstone disease, the gallbladder becomes the target organ of a complex metabolic disease. Indeed, a fine coordinated hepatobiliary and gastrointestinal function, including gallbladder motility in the fasting and postprandial state, is of crucial importance to prevent crystallization and precipitation of excess cholesterol in gallbladder bile. Also, gallbladder itself plays a physiopathological role in biliary lipid absorption. Here, we present a comprehensive view on the regulation of gallbladder motor function by focusing on recent discoveries in animal and human studies, and we discuss the role of the gallbladder in the pathogenesis of gallstone formation. 47:2112-2126 G allstones are one the most common gastrointestinal diseases that require hospitalization in the western world, 1 and this is a true health burden 2-4 with enormous costs estimated at 6.5 billion dollars each year in United States. 4,5 Because life expectancy and the incidence rate of obesity are both rising worldwide, 6 the incidence rate of gallstones may increase, often in the context of the "metabolic syndrome". 7 The estimated prevalence of gallstones is 10%-15% in the general population of developed countries. In the United States, approximately 20 million to 25 million adults have gallstones. The burden of the disease is highest (60%-70%) in American Indians followed by Hispanics of mixed Indian origin. In contrast, the rate is lowest (less than 5%) in Asian and African populations. 5 The prevalence is intermediate (10%-15%) in Caucasians in developed countries. In Europe, the Multicenter Italian Study on Cholelithiasis (MICOL) ultrasonographic survey, which was performed across Italy including 29,000 subjects aged 30-69 years, reported an overall prevalence rate of 18.8% and 9.5% in women and men, respectively. 8 Major risk factors for the development of gallstones have been better identified over the past years and include age, female sex, some genetic polymorphisms within a background of a complex genetic disorder, pregnancy, obesity and rapid weight loss on low caloric diets or fol-

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Endothelin receptors in human and guinea-pig gallbladder muscle

Cited by 26 publications

References 28 publications

Endothelin Receptors in Gastrointestinal Smooth Muscle

Endothelin Receptors in Gastrointestinal Smooth Muscle

Smooth muscle function and dysfunction in gallbladder disease

Coordinate regulation of gallbladder motor function in the gut-liver axis

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