Extracellular K+ Effects on the Mouse Aortic Endothelial Cell Contractility / 대한흉부외과학회지

ABSTRACT

BACKGROUND: External stimuli increases intracellular (IC) Ca2+, which increases extracellular (EC) K+. To verify K+ effects on the vascular contraction, we performed an experiment using mouse aortic endothelial cell. MATERIAL AND METHOD: We examined the mouse aortic contractility changes as we measured the IC Ca2+ change and ionic current by using the voltage clamp technique under different conditions such as; increasing EC K+, removing endothelial cell, giving L-NAME (N-nitro-L-arginine methyl ester) which suppress nitric oxide formation, Ouabain which control Na+-K+ pump and Ni2+ which repress Na+-Ca2+ exchanger. RESULT: When we increased EC K+ from 6 to 12 mM, there was no change in aortic contractility. Aorta contracted with more than 12 mM of EC K+. Acetylcholine (ACh) induced relaxation was inhibited with EC K+ from 6 to 12 mM, but was not found after de- endothelialization or L-NAME treatment. ATP or ACh increased IC Ca2+ in cultured endothelium. After maximal increase of IC Ca2+, increasing EC K+ from 6 to 12 mM made IC Ca2+ decrease and re-decreasing EC K+ to 6 mM made IC Ca2+ increase. Ouabain and Ni2+ masked the inhibitory effect of endothelium dependent relaxation by increased EC K+. CONCLUSION: These data indicate that increase in EC K+ relaxes vascular smooth muscle and reduces Ca2+ in the endothelial cells which inhibit endothelium dependent relaxation. This inhibitory mechanism may be due to the activation of Na+-K+ pump and Na+-Ca2+ exchanger.