Extracellular K+ Effects on the Mouse Aortic Endothelial Cell Contractility.
- Author:
Jae Ho AHN
1
;
Ji Young YOU
Author Information
1. Department of Thoracic & Cardiovascular Surgery, Mokdong Hospital, Ewha Women's University, Korea. jhahn@mm.ewha.ac.kr
- Publication Type:Original Article
- Keywords:
Endothelium;
Endothelium-dependent relaxing factor;
Potassium
- MeSH:
Acetylcholine;
Adenosine Triphosphate;
Animals;
Aorta;
Endothelial Cells*;
Endothelium;
Endothelium-Dependent Relaxing Factors;
Masks;
Mice*;
Muscle, Smooth, Vascular;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Ouabain;
Potassium;
Relaxation
- From:The Korean Journal of Thoracic and Cardiovascular Surgery
2003;36(12):887-893
- CountryRepublic of Korea
- Language:Korean
-
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.
