Figure 4 | Scientific Reports

Figure 4

From: Acute-on-chronic liver disease enhances phenylephrine-induced endothelial nitric oxide release in rat mesenteric resistance arteries through enhanced PKA, PI3K/AKT and cGMP signalling pathways

Figure 4

(A) Phenylephrine-induced NO release in mesenteric resistance arteries from sham-operated (SO) and microsurgical liver cholestasis (LC) rats. Influence of preincubation with the specific iNOS inhibitor 1400 W (1 μmol/L), the unspecific NOS inhibitor L-NAME (100 μmol/L), the PI3K inhibitor LY 294002 (10 μmol/L) and the PKA inhibitor H89 (1 μmol/L). Data were expressed as arbitrary fluorescence units/mg tissue. n = 6–16 segments from different animals in each group. (B) Western blot analysis for total and phosphorylated endothelial nitric oxide synthase (eNOS) in the Ser 1177 residue (P-eNOS) and inducible nitric oxide synthase (iNOS) in mesenteric resistance arteries from SO and LC rats. Each lane is representative of 8 isolated arterial segments from different animals in each group. Endothelial cells were used as a positive control (+C) for both eNOS and P-eNOS analysis. Activated macrophages were used as a positive control (+C) for iNOS analysis. Lower panel shows the densitometric analyses for the expression of each protein. Results (mean ± S.E.M.) were expressed as the relation between the signal obtained for the protein analysed and the signal obtained for β-actin.

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