Abstract: 240 Avian-2000 commercial broilers were allocated equally into a normal temperature control group (NT), a low temperature group (LT) and a low temperature with supplemental L-arginine group (LA) at day 14 of age. Starting on day 14, birds in groups LA and LT were subjected to the same low temperature by lowing 1~2 °C per day from 28 °C (d 14) down to 12~14 °C (d 21), and remained constant until day 49. Starting on day 14, an additional 100 mg/kg L-arginine was added to the basal diets of group LA. Incidence of pulmonary hypertension syndrome (PHS) was recorded. Right/total ventricle ratio (RV/TV), plasma nitric oxide (NO), vessel wall area to vessel total area ratio (WA/TA), and mean media thickness of pulmonary arterioles (mMTPA) were measured at days 24, 32, 39 and 45 of age. Apoptosis of smooth muscle cells in pulmonary arterioles were detected using TdT-mediated dUTP-biotin nick end labeling (TUNEL) kit. It was found that birds in the group LT had increased PHS incidence, RV/TV, WA/TA and mMTPA compared with those in the group NT. Birds in the group LA tended to have lower WA/TA and mMTPA than those in the group LT, and this tendency was pronounced on day 32. Plasma NO concentration was increased in the group LA compared to that in the groups NT and LT from days 32 to 45, but there were no differences between the groups LT and NT despite an exception on day 39. Birds in the group LA had increased apoptotic to total smooth muscle cells ratio than those in the groups NT and LT; however, there were no differences between the groups LT and NT. It was demonstrated that L-arginine/NO promoted apoptosis in pulmonary smooth muscle cells and thereby prevented pulmonary vascular remodeling to a certain extent.