Phenotype, intestinal morphology, and survival of homozygous and heterozygous endothelin B receptor–deficient (spotting lethal) rats

Possible Protection of Sinusoidal Endothelial Cells by Endothelin B Receptor During Hepatic Warm Ischemia–Reperfusion

“…17 ETB-Rs are present in almost all organs and tissues, and they do not only counteract the vasoconstrictor effect of ET-1, but they also serve to eliminate either circulating or extracellular ET-1. 18 In the present study, the ET-1 levels in the +/+ rats were lower than those in the sl/sl rats before ischemia because ETB-R might remove ET-1. At 2 h after reperfusion, the ET-1 levels increased because of I/R injury in both the sl/sl and the +/+ rats, and yet, the levels in the sl/sl rats were higher than those in the +/+ rats.…”

“…5,7,28,29 ETB-R is expressed in a wide variety of tissues, including the brain, kidney, lung, heart, endothelial cell, and vascular smooth muscle along with the liver. 17,18 In the liver, ETB-R occurs in SECs, hepatic stellate cells, and Kupffer cells. 12,15 To reveal the role of ETB-R in hepatic microcirculation, various antagonists and agonists have been examined in previous studies; however, the results of such studies varied and the exact roles thus remain obscure.…”

“…16 However, the length of aganglionic segments varies in individual rats. 18 The long type aganglionosis rats lapse into an abdominal distension within 4 weeks, on the other hand, the short type aganglionosis rats survive over several months. Both macroscopic and routine histological examinations of the sl/sl rats showed no abnormalities in the heart, aorta, brain, liver, lung, kidney, adrenal glands, or urinary bladder.…”

“…Both macroscopic and routine histological examinations of the sl/sl rats showed no abnormalities in the heart, aorta, brain, liver, lung, kidney, adrenal glands, or urinary bladder. 18 We herein evaluated the pure biological role of ETB-R regarding the development of hepatic warm I/R injury using congenital ETB-R defi cient spotting lethal (sl) rats.…”

Possible involvement of muscularis resident macrophages in impairment of interstitial cells of Cajal and myenteric nerve systems in rat models of TNBS-induced colitis

“…In intestinal aganglionosis in Hirschsprung's disease, alteration of the myenteric nerve system might lead to a disturbance of colonic peristaltic motor function (Holschneider et al 1994;Howard et al 1984). This phenomenon has also been conWrmed in an endothelin ET B receptor-deWcient rat model of Hirschsprung's disease (Dembowski et al 2000;von Boyen et al 2002;Won et al 2002).…”