Aim:To explore the role of carbon monoxide(CO)in the regulation of hypoxicpulmonary artery smooth muscle cell(PASMC)proliferation and apoptosis bynitric oxide(NO).Methods:PASMC of Wistar rats was cultured in vitro in thepresence of a NO donor,sodium nitroprusside,or an inhibitor of heine oxygenase(HO),zinc protoporphyrin-IX,or under both normoxic and hypoxic conditions.Nitrite and carboxyhemoglobin in PASMC medium were detected withspectrophotometry.The proliferating and apoptotic percentage of PASMC wasmeasured by flow cytometry.The expression of HO-1 mRNA in PASMC wasanalyzed by fluorescent real-time quantitative PCR,and the proliferating cell nuclearantigen and caspase-3 were examined by immunocytochemical analysis.Results:The results showed that hypoxia suppressed NO generation from PASMC,whichpromoted hypoxic PASMC proliferation and induced apoptosis.Meanwhile,hy-poxia induced HO-1 expression in PASMC and promoted CO production fromPASMC,which inhibited PASMC proliferation and regulated PASMC apoptosis.NO upregulated the expression of HO-1 mRNA in hypoxic PASMC;NO also inhib-ited proliferation and promoted apoptosis of hypoxic PASMC,possibly by regu-lating the production of CO.Conclusion:The results indicated that CO couldinhibit proliferation and regulate apoptosis of PASMC,and NO inhibited prolifera-tion and promoted apoptosis of hypoxic PASMC,possibly by regulating the pro-duction of CO. Aim: To explore the role of carbon monoxide (CO) in the regulation of hypoxic pulmonary artery smooth muscle cell (PASMC) proliferation and apoptosis by nitric oxide (NO). Methods: PASMC of Wistar rats was cultured in vitro in the presence of a NO donor, sodium nitroprusside, or an inhibitor of heine oxygenase (HO), zinc protoporphyrin-IX, or under both normoxic and hypoxic conditions. Nitrite and carboxyhemoglobin in PASMC medium were detected with spectrophotometry. proliferating and apoptotic percentage of PASMC wasmeasured by flow cytometry. expression of HO-1 mRNA in PASMC wasanalyzed by fluorescent real-time quantitative PCR, and the proliferating cell nuclearantigen and caspase-3 were examined by immunocytochemical analysis. Results: The results showed that hypoxia inhibited NO generation from PASMC, which promoted hypoxic PASMC proliferation and induced apoptosis. Meanwhile, hy-poxia induced HO-1 expression in PASMC and promoted CO production from PASMC, which inhibited PASMC proliferation and reg ulated PASMC apoptosis. NO upregulated the expression of HO-1 mRNA in hypoxic PASMC; NO also inhib-ited proliferation and promoted apoptosis of hypoxic PASMC, possibly by regu-lating the production of CO.Conclusion: The results indicated that CO could inhibit proliferation regulate apoptosis of PASMC, and NO regulated prolifera tion and promoted apoptosis of hypoxic PASMC, possibly by regulating the pro-duction of CO.