Korean J Thorac Cardiovasc Surg.
2003 Dec;36(12):887-893.
Extracellular K+ Effects on the Mouse Aortic Endothelial Cell Contractility
- Affiliations
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- 1Department of Thoracic & Cardiovascular Surgery, Mokdong Hospital, Ewha Women's University, Korea. jhahn@mm.ewha.ac.kr
- 2Department of Emergency Medicine, Kangdong Sacred Heart Hospital, Hallym University, Korea.
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.
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.