N-acetyl cysteine’s (NAC) anti-inflammatory, antioxidant and vasodilator effects are well known. However, explaining the mechanism of the effects are not sufficient. In this study, on the vasodilatory effect of NAC, role of ATP-sensitive potassium (KATP) channel was investigated by using electrophysiological and molecular genetics methodologies. In this study, aorta smooth muscle cell lines were used. One con trol and three dose groups were studied. The control group were not exposed any treatment. The dose groups were treated with 2, 5 and 10 mMNACrespectively, using the cellattached patch clamp KATP channel currents were measured for 10 min. Intracellular calcium levels in the same groups has been monitored using confocal laser scanning microscope by taking images at 488 nm wavelength with 15 s intervals for 10 min. KATP channel gene expression levels were assayed using real-time quantitative reverse transcription polymerase chain reaction. KATP channel gene expression (Kcnj8, Kcnj11, Abcc8, Abcc9) levels for each group were determined. KATP channel flow was significantly increased in all dose groups compared to the control group. However, significant dif ferences were not found among dose groups. Although, intracel lular calcium concentrations relative to control group did not change in 2 and 5 mM groups, significant reduction was observed in 10 mM group. Compared to control group, Kcnj8 gene expression levels of 2 and 10 mM groups observed to be decreased, while there was not a significant difference between groups in the proportion of Kcnj11 expression. Abcc8 gene expression rate decreased in only 2 mM group relative to control group. While, in the 2 and 10 mM groups, compared to the con trol group, Abcc9 expression levels were significantly increased, no significant change were observed in 5 mM group. Results obtained in this study suggested that, NAC’s vasodila tory effect may be associated with KATP channels. This relation ship has been showed for the first time.