The Proatherogenic Effect of Chronic Nitric Oxide Synthesis Inhibition in ApoE-Null Mice Is Dependent on the Presence of PPARα

Figure 5

Proposed mechanism for the collusion of PPARα and AII in the ApoE-null mouse with wild type (WT) PPARα gene. The preferential eNOS activity inhibition by low dose L-NAME is suggested to alter the balance between AII and endothelium-derived NO, allowing amplification of the proatherogenic effect of unopposed AII action.