Objective: The present study was conducted to examine the activity of protein kinase Cα (PKCα) in the pulmonary arterioles of broilers during the pathophysiological progression leading to pulmonary hypertension on one hand and the association between activation of PKCα and pulmonary vascular remodeling on the other hand. Method: One hundred and sixty Avian-2000 broilers were divided equally into control group and cold temperature group. All the birds were reared according to normal temperature schedule before day 14, and the lighting schedule provided 24h light per day. Thereafter, birds in cold temperature group were subjected to low temperature by lowering 1~2 °C per day to 14~12°C, and then remained constant until day 49, while birds in control group were still brooded at standard temperature. All the birds received pelleted diet throughout the study. Samples of heart, blood and lung were collected at day 24,32,39,45 of age, respectively. Right ventricle to total ventricle ratio (RV/TV) and packed cell volume (PCV) were measured. Vessel wall area to vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA) was examined using computer-image analytic software. Expression of PKC in pulmonary muscular arterioles was investigated by immunohistochemistry technique, and quantified by measuring optical density (OD) using computer-image analytic software. Results: Incidence of pulmonary hypertension syndrome (PHS) amounted to 12.5% in birds exposed to cold, which was fairly high compared to 3.75% of the control group (P<0.05). PCV elevated after day 32 (P<0.05), and RV/TV ratio increased on day 45 (P<0.05). Both the WA/TA and mMTPA of birds subjected to cold were significantly elevated when compared with that of control group during every individual’s life span (P<0.05). The OD values showed an upward trend but did not significant increase before day 32 (P>0.05), however, one week later (at day 39 of age), there was a much larger rise in broilers kept under cold temperature and the difference between the two groups was very pronounced (P<0.05). There was still a trend on day 45 although the difference was less significant (P>0.05). The increased PKCα expression was positively correlated with the values of mMTPA and WA/TA. Conclusion: PKCα expression was up regulated to a certain extent during the pathophysiological progression leading to pulmonary hypertension, and activation of PKCα might be involved in the development of pulmonary vascular remodeling.