Effects of the Rho-Kinase Inhibitor, Fasudil, on Pulmonary Hypertension

motility, migration, proliferation, differentiation, and apoptosis. Activation of Rho/ROCK is considered to play a major role in the pathogenesis of several cardiovascular diseases, including PH,5 and thus is a new therapeutic target for PH (Figure). Fasudil is one of the most frequently used ROCK inhibitors, and was approved as a therapeutic agent for vasospasm after arachnoid hemorrhage. Several studies reported that fasudil ameliorated PH in various animal models, including PH induced by monocrotaline (MCT), Sugen5416/hypoxia, and bleomycin.6–10 Oka et al demonstrated the effects of acute ROCK inhibition by intravenous administration of fasudil on Sugen5416/hypoxia-induced PH in rats.10 Intravenous fasudil was more effective in reducing right ventricular systolic pressure (RVSP) compared with ulmonary hypertension (PH) is a progressive, lifethreatening disease characterized by vasoconstriction, thrombosis, and vascular remodeling, leading to elevated pulmonary arterial pressure (PAP), right heart failure and death. Vasorelaxant agents, including prostanoids, phosphodiesterase-5 (PDE-5) inhibitors, and endothelin receptor antagonists (ERAs), have been shown to improve symptoms, exercise tolerance, and mortality in PH patients.1–3