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. Author manuscript; available in PMC: 2011 Nov 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2010 Nov;56(5):471–474. doi: 10.1097/FJC.0b013e3181fa8e20

Figure.

Figure

Pathophysiological mechanisms and molecular targets in MCT-treated and hypoxia-induced model of PAH. The PAH-associated endothelial cell dysfunction and decreased pulmonary artery relaxation, and the VSM dysfunction and increased pulmonary artery constriction and remodeling are reduced by treatment with the PDE inhibitor sildenafil, or the ET-1 receptor antagonist bosentan. 2-ME enhances the stimulatory effects of sildenafil on pulmonary artery relaxation, and the inhibitory effects of bosentan on vasoconstriction and remodeling.