):A1-A306 A191 BSG abstracts dependent-magnetic resonance imaging (BOLD-MRI) was used to quantify changes in renal oxygenation. Tissue expression and distribution of RLN receptor (RXFP1) was determined by qPCR and immunofluorescence. Expression of vasoconstrictor genes was quantified by qPCR array. Results RXFP1 was detected on glomerular podocytes, renal pericytes, and endothelial cells of the renal, segmental and interlobar arteries of cirrhotic rats. In CCl 4 cirrhosis, acute i.v. RLN (4µg) induced a 50% increase in RBF after 60 minutes (p < 0.01 vs. placebo, n = 6). BOLD-MRI showed increased tissue oxygenation at the same timepoint in renal cortex and medulla. Extended s.c. RLN increased RBF by 54% in CCl 4 (p < 0.01 vs. placebo, n = 8) and 57% in BDL (p < 0.001 vs. placebo, n = 5) and increased GFR by 138% in CCl 4 (p < 0.01 vs. placebo, n = 8) and 103% in BDL (p < 0.05 vs. placebo, n = 5). Mean arterial pressure was unaffected by RLN. L-NAME (250mg/L) orally (p.o.) abrogated the effect of RLN on RBF and GFR. The relative expression of vasoconstrictor genes in the kidney was markedly reduced by RLN treatment. Conclusion RLN increases RBF in experimental cirrhosis. Crucially, RLN also improves renal function and oxygenation but does not induce systemic hypotension even in decompensated disease. The effects of RLN are mediated via augmentation of NO and downregulation of vasoconstrictor genes known to be important in the pathogenesis of HRS. RLN has potential as a treatment for HRS and further translational studies are warranted. Disclosure of Interest None Declared.

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