Background The RhoNRho kinase pathway may participate in the pathogenesis of hypoxia and monocrotalineinduced pulmonary hypertension.This study tested whether RhoNRho kinase pathway is involved in the pathogenesis ofhigh flow induced pulmonary hypertension in rats.Methods Male Wistar rats(4 weeks)were randomly divided into 4 shunt groups,4 treated groups and 4 control groups.Shunt and treated groups underwent left common carotid artery/external jugular vein shunt operation.Control groupsunderwent sham operation.Treated groups received fasudil treatment and the others received same dose of saline.Atweeks 1,2,4 and 8 of the study,right ventricular systolic pressure was measured and blood gases were analysed tocalculate Qp/Qs.The weight ratio of right ventricle to left ventricle plus septum and the mean percentage of medial wallthickness in moderate sized pulmonary arteries were obtained.RhoA activity in pulmonary arteries was detected usingRho activity assay reagent.Rho kinase activity was quantified by the extent of MYPT1 phosphorylation with Western blot.Proliferating cells were evaluated using proliferating cell nuclear antigen immunohistological staining.Results Carotid artery/jugular vein shunt resulted in high pulmonary blood flow,both an acute and a chronic elevationof right ventricular systolic pressure,significant medial wall thickening characterized by smooth muscle cells proliferation,right ventricular hypertrophy and increased activation of RhoA and Rho kinase.Fasudil treatment lowered pulmonaryartery systolic pressure,suppressed pulmonary artery smooth muscle cells proliferation,attenuated pulmonary arterymedial wall thickening and inhibited right ventricular hypertrophy together with significant suppression of Rho kinaseactivity but not Rho activity.Conclusions Activated RhoNRho kinase pathway is associated with both the acute pulmonary vasoconstriction andthe chronic pulmonary artery remodelling of high flow induced pulmonary hypertension.Fasudil treatment could improvepulmonary hypertension by inhibiting Rho kinase activity. Background The RhoNRho kinase pathway may participate in the pathogenesis of hypoxia and monocrotaline induced pulmonary pleigensis. This study tested whether RhoNRho kinase pathway is involved in the pathogenesis of high flow induced pulmonary hypertension in rats. Male Male Wistar rats (4 weeks) were randomly divided into 4 shunt groups, 4 treated groups and 4 control groups. Shunt and treated groups underwent left common carotid artery / external jugular vein shunt operation. Control groups underwent sham operation. Treated groups received fasudil treatment and the others received the same dose of saline. Atweeks 1,2 , 4 and 8 of the study, right ventricular systolic pressure was measured and blood gases were analyzed tocalculate Qp / Qs.The weight ratio of right ventricle to left ventricle plus septum and the mean percentage of medial wallthickness in moderate sized pulmonary arteries were obtained. RhoA activity in pulmonary arteries was detected using Rho activity assay reagent. Rho kinase activity w as quantified by the extent of MYPT1 phosphorylation with Western blot. Proliferating cells were evaluated using proliferating cell nuclear antigen immunohistological staining. Results of Carotid artery / jugular vein shunt resulted in high pulmonary blood flow, both an acute and a chronic elevation of right ventricular systolic pressure, significant medial wall thickening characterized by smooth muscle cells proliferation, right ventricular hypertrophy and increased activation of RhoA and Rho kinase. Fasudil treatment demonstrating reduced pulmonary artery systolic pressure, suppressed pulmonary artery smooth muscle cells proliferation, attenuated pulmonary artery medial wall thickening and inhibited right ventricular hypertrophy together with significant suppression of Rho kinase activity but not Rho activity. Conclusions Activated RhoNRho kinase pathway is associated with both the acute pulmonary vasoconstriction and the chronic pulmonary artery remodeling of high flow induced pulmonary hypertension. Fasudil treatment could improvepulmonary hypertension by inhibiting Rho kinase activity.