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In this study, we aimed to investigate the role of ATP-sensitive potassium (KATP) channel, Na+/K+-ATPase activity, and intracellular calcium levels on the vasodilatory effect of N-acetylcysteine (NAC) in thoracic aorta by using electrophysiological and molecular techniques.

Background: In this study, we aimed to investigate the role of ATP-sensitive potassium (KATP) channel, Na+/K+-ATPase activity, and intracellular calcium levels on the vasodilatory effect of N-acetylcysteine (NAC) in thoracic aorta by using electrophysiological and molecular techniques. Methods: Rat thoracic aorta ring preparations and cultured thoracic aorta cells were divided into four groups as control, 2 mM NAC, 5 mM NAC, and 10 mM NAC. Thoracic aorta rings were isolated from rats for measurements of relaxation responses and Na+/K+-ATPase activity. In the cultured thoracic aorta cells, we measured the currents of KATPchannel, the concentration of intracellular calcium and mRNA expression level of KATPchannel subunits (KCNJ8, KCNJ11, ABCC8 and ABCC9). Results: The relaxation rate significantly increased in all NAC groups compared to control. Similarly, Na+/K+-ATPase activity also significantly decreased in NAC groups. Outward KATPchannel current significantly increased in all NAC groups compared to the control group. Intracellular calcium concentration decreased significantly in all groups with compared control. mRNA expression level of ABCC8 subunit significantly increased in all NAC groups compared to the control group. Pearson correlation analysis showed that relaxation rate was significantly associated with KATPcurrent, intracellular calcium concentration, Na+/K+-ATPase activity and mRNA expression level of ABCC8 subunit. Conclusion: Our findings suggest that NAC relaxes vascular smooth muscle cells through a direct effect on KATPchannels, by increasing outward K+flux, partly by increasing mRNA expression of KATPsubunit ABCC8, by decreasing in intracellular calcium and by decreasing in Na+/K+-ATPase activity.