Pulmonary hypertension (PH) is characterised by progressive elevation of pulmonary artery pressure and pulmonary vascular resistance. Pathohistological findings have demonstrated that PH is associated with abnormal vascular structures, including medial and/or intimal hypertrophy, concentric or eccentric intimal fibrosis, obstruction in the arterial lumen, and aneurysmal dilatation.¹ Patients with PH are currently treated with anticoagulant agents, vasodilators including continuous intravenous prostacyclin (prostaglandin I₂) and oral sildenafil or bosentan, and in end stage, with lung transplantation,¹ when applicable. Endothelial dysfunction of pulmonary arteries and enhanced pulmonary vasoconstriction contribute to the development of PH.¹ Endothelial nitric oxide synthase (eNOS) expression is reduced in patients with PH and therefore nitric oxide inhalation and sildenafil are useful for those patients. However, more effective treatments remain to be developed.¹

We have recently demonstrated that Rho-kinase is substantially involved in the pathogenesis of a wide range of cardiovascular disease.^2,3 Rho-kinase suppresses myosin phosphatase activity by phosphorylating the myosin binding …