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AIM:To delineate the mechanisms of renal vasoconstriction in hepatorenal syndrome (HRS),we investigated the expression of type Ⅰ inositol 1,4,5-triphosphate receptors (IP3R Ⅰ) of kidney in mice with fulminant hepatic failure (FHF).METHODS:FHF was induced by lipopolysaccharide (LPS) in D-galactosamine (GaIN) sensitized BALB/c mice.There were 20 mice in normal saline (NS)-treated group,20 mice in LPS-treated group,20 mice in GaINtreated group,and 60 mice in GaIN/LPS-treated group (FHF group).Liver and kidney tissues were obtained at 2,6,and 9 h after administration.The liver and kidney specimens were stained with hematoxylin-eosin for studying morphological changes under light microscope.The expression of IP3R Ⅰ in kidney tissue was tested by immunohistochemistry,West blot and reverse transcription (RT)-PCR.RESULTS:Kidney tissues were morphologically normal at all time points in all groups.IP3R Ⅰ proteins were found localized in the plasma region of glomerular mesangial cells (GMC) and vascular smooth muscle cells (VSMC) in kidney by immunohistochemical staining.In kidney of mice with FHF at 6 h and 9 h IP3R Ⅰ staining was upregulated.Results from West blot demonstrated consistent and significant increment of IP3R Ⅰ expression in mice with FHF at 6 h and 9 h (t = 3.16,P＜0.05;t = 5.43,P＜0.01).Furthermore,we evaluated IP3R Ⅰ mRNA expression by RT-PCR and observed marked upregulation of IP3R Ⅰ mRNA in FHF samples at 2 h,6 h and 9 h compared to controls (t = 2.97,P＜0.05;t = 4.42,P＜0.01;t = 3.81,P＜0.01).CONCLUSION:The expression of IP3R Ⅰ protein increased in GMC and renal VSMC of mice with FHF,possibly caused by up-regulation of IP3R Ⅰ mRNA.