Endothelial nitric oxide synthase is not essential for the development of fibrosis and portal hypertension in bile duct ligated mice

Koshy, A; De Gottardi, A; Ledermann, M; Saegesser, H; Shaw, SG; Zimmermann, A; Reichen, J (2005). Endothelial nitric oxide synthase is not essential for the development of fibrosis and portal hypertension in bile duct ligated mice. Liver international, 25(5), 1044-52.. Oxford: Blackwell Munksgaard 10.1111/j.1478-3231.2005.01146.x

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BACKGROUND/AIMS: It is postulated that nitric oxide (NO) is responsible for the hyperdynamic circulation of portal hypertension. Therefore, we investigated induction of fibrosis and hyperdynamic circulation in endothelial NO synthase knock-out (KO) mice. METHODS: Fibrosis was induced by bile duct ligation. Hemodynamic studies were performed after portal vein ligation. All studies were performed in wild-type (WT) and KO mice. RESULTS: Three to 4 weeks after bile duct ligation (BDL), both WT and KO groups had similar degrees of portal hypertension, 12 (9-14) and 11(8-15) mmHg, median (range), and liver function. Fibrosis increased from 0.0% in sham operated to 1.0 and 1.1% in WT and KO mice, respectively. Cardiac output was similar after portal vein ligation (20 and 17 ml/min in WT and KO mice, respectively). There was no difference in liver of mRNA for endothelin 1, inducible NO synthase (iNOS) and hem-oxygenase 1 (HO1); proteins of iNOS, HO1 and HO2; nor in endothelin A and B (EtA and EtB) receptor density between WT and KO mice after BDL. CONCLUSIONS: These results suggest that endothelial NO synthase is neither essential for the development of fibrosis and portal hypertension in bile duct ligated mice, nor for the hyperdynamic circulation associated with portal hypertension in the portal vein ligated mice.

Item Type:	Journal Article (Original Article)
Division/Institute:	04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DCR Unit Tiefenau Hospital [discontinued] > Forschungsgruppe Vasoaktive Peptide [discontinued]
UniBE Contributor:	Shaw, Sidney
ISSN:	1478-3223
ISBN:	16162165
Publisher:	Blackwell Munksgaard
Language:	English
Submitter:	Factscience Import
Date Deposited:	04 Oct 2013 14:58
Last Modified:	05 Dec 2022 14:18
Publisher DOI:	10.1111/j.1478-3231.2005.01146.x
PubMed ID:	16162165
Web of Science ID:	000231825700019
URI:	https://boris.unibe.ch/id/eprint/25000 (FactScience: 54600)