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KMID : 0364020030360120887
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Korean Journal of Thoracic and Cardiovascular Surgery
2003 Volume.36 No. 12 p.887 ~ p.893
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Extracellular K+ Effects on the Mouse Aortic Endothelial Cell Contractility
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Ahn Jae-Ho
Yoo Ji-Young
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Abstract
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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. Meterial 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 deendothelialization 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.
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KEYWORD
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Endothelium, Endothelium-dependent relaxing factor, Potassium
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