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. Author manuscript; available in PMC: 2009 Aug 11.
Published in final edited form as: Hepatology. 2008 May;47(5):1754–1763. doi: 10.1002/hep.22203

Figure 5. Regulation of intrahepatic NO generation in liver cirrhosis and portal hypertension.

Figure 5

One of the most well established defects in SEC-HSC crosstalk in liver injury is the decreased bioavailability of the vasodilator NO. which occurs independent of changes in eNOS expression and through defects in post-translational regulation of the enzyme within endothelial cells. During the process of liver injury, reduction of NO bioavailability occurs due to decreased synthesis of NO, enhanced inactivation of NO by the overproduction of superoxide (O2−) or both. An inactivation of eNOS occurs through an increase in cav-1 expression as well as one recently recognized protein, the G-protein-coupled receptor kinase 2 (GRK2), which directly interacts with and inhibits Akt, thereby decreasing eNOS activity.