Aim:To study the effect of 5-hydroxydecanoate (5-HD) on the proliferation of 24h hypoxic human pulmonary artery smooth muscle cells (HPASMC) and to explorethe pharmacological mechanisms of 5-HD as an inhibitor of mitochondrial mem-brane ATP-sensitive potassium channel activation.Methods:Normoxic or hy-poxic HPASMC in culture were stimulated by either diazoxide or 5-HD for 24 h.The proliferation of HPASMC was examined by 3-(4,5-dimethyl-2-thiazol-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and proliferating cell nuclear anti-gen (PCNA) immunohistochemistry staining.The apoptosis of HPASMC wasassessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end la-beling (TUNEL) assayand flow cytometric analysis.The relative changes inmitochondrial membrane potential (ΔΨ_m) were measured using the rhodamine fluo-rescence (R-123) technique.Results:Both hypoxia and diazoxide stimulationincreased ΔΨ_m value measured by the absorbance of MTT,PCNA-positive stain-ing and decreased TUNEL-positive staining and apoptotic cells in HPASMC.Hypoxia and the concomitant stimulation of diazoxide obviously enhanced theeffects of hypoxia or diazoxide alone.5-HD significantly attenuated the effects ineach of the above conditions.Additionally,5-HD partially inhibited the effect ofhypoxia on R-123 fluorescence intensity in HPASMC.Conclusion:5-HD caninhibit the proliferation of hypoxic HPASMC by blocking mitochondrial K_(ATP)channels. Aim: To study the effect of 5-hydroxydecanoate (5-HD) on the proliferation of 24h hypoxic human pulmonary artery smooth muscle cells (HPASMC) and to explore the pharmacological mechanisms of 5-HD as an inhibitor of mitochondrial mem-brane ATP- sensitive potassium channel activation. Methods: Normoxic or hy-poxic HPASMC in culture were stimulated either either diazoxide or 5-HD for 24 h. The proliferation of HPASMC was examined by 3- (4,5-dimethyl-2-thiazol- yl) 2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and proliferating cell nuclear anti-gen (PCNA) immunohistochemistry staining. The apoptosis of HPASMC was identified by terminal deoxynucleotidyl transferase-mediated dUTP nick end la- beling (TUNEL) assay and flow cytometric analysis. The relative changes in mitochondrial membrane potential (ΔΨ_m) were measured using the rhodamine fluo-rescence (R-123) technique. Results: Both hypoxia and diazoxide stimulation in- creased ΔΨ_m value measured by the absorbance of MTT, PCNA-positive stain- ed TUNEL-positive staining and apoptotic cells in HPASMC. Hypoxia and the concomitant stimulation of diazoxide obviously enhanced the effects of hypoxia or diazoxide alone. 5-HD significantly attenuated the effects ineach of the above conditions. Additionally, 5-HD partially inhibited the effect of hypoxia on R-123 fluorescence intensity in HPASMC. Confluence: 5-HD caninhibit the proliferation of hypoxic HPASMC by blocking mitochondrial K ATP channels.