Introduction: It has been recognized that the sympathetic nervous system is activated in pulmonary arterial hypertension (PAH), and abnormal sympathetic hyperactivity leads to worsening of PAH via endothelial dysfunction. The purpose of this study was to examine whether sympathetic ganglion block (SGB) can treat PAH by increasing the availability of nitric oxide (NO). Methods: Male Sprague-Dawley rats were allocated into 3 groups that received daily injections of 0.1 ml of saline (control and monocrotaline (MCT) groups) or 0.25% ropivacaine (SGB-MCT group) into the left superior cervical ganglion for 28 days after subcutaneous administration of saline (control group) or 50 mg/kg of MCT (MCT and SGB-MCT groups). Heart rate variability was recorded to assess autonomic activity. Right ventricular systolic pressure and hypertrophy were evaluated after sacrifice. Lung tissue NO synthase, arginase, and oxidative stress were examined. Microscopic exam was done to evaluate pulmonary arterial hypertrophy. Results: PAH was evident in the MCT group, with right ventricular systolic pressures (47 ± 11 mmHg) that were higher than those of controls (17 ± 5 mmHg), while SGB significantly attenuated MCT-induced PAH (28 ± 4 mmHg). The right/left ventricular mass ratios exhibited similar changes to those seen with right ventricular pressures. Heart rate variability showed significantly higher sympathetic activity in the MCT group. Additionally, microscopy revealed a higher proportion of muscular arteries with thicker medial walls in the MCT group, which was attenuated by SGB. MCT also induced arginase hyperactivity, which was in turn decreased by SGB-induced endothelial NO synthase activity. SGB restored hypoactivity of superoxide dismutase and increased malondialdehyde and nitrotyrosine induced by MCT. Conclusions: SGB could suppress PAH and the remodeling of pulmonary arteries via inactivation of arginase and reciprocal elevation of NO bioavailability, thus attenuating disproportionate hyperactivation of the sympathetic nervous system.