HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/1/H329    most recent 00503.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Seol, G. H. Articles by Suh, S. H. Search for Related Content PubMed PubMed Citation Articles by Seol, G. H. Articles by Suh, S. H.

Inhibition of endothelium-dependent vasorelaxation by extracellular K⁺: a novel controlling signal for vascular contractility

¹Department of Physiology and Medical Research Center, College of Medicine, Ewha Women's University, ²Department of Physiology, College of Medicine, Dankook University, Seoul 158-710, Republic of Korea; and ³Laboratorium voor Fysiologie, Campus Gasthuisberg, Katholieke Universiteit, Leuven, B-3000 Leuven, Belgium

Submitted 4 June 2003 ; accepted in final form 4 September 2003

The effects of extracellular K⁺ on endothelium-dependent relaxation (EDR) and on intracellular Ca²⁺ concentration ([Ca²⁺]_i) were examined in mouse aorta, mouse aorta endothelial cells (MAEC), and human umbilical vein endothelial cells (HUVEC). In mouse aortic rings precontracted with prostaglandin F₂ or norepinephrine, an increase in extracellular K⁺ concentration ([K⁺]_o) from 6 to 12 mM inhibited EDR concentration dependently. In endothelial cells, an increase in [K⁺]_o inhibited the agonist-induced [Ca²⁺]_i increase concentration dependently. Similar to K⁺, Cs⁺ also inhibited EDR and the increase in [Ca²⁺]_i concentration dependently. In current-clamped HUVEC, increasing [K⁺]_o from 6 to 12 mM depolarized membrane potential from –32.8 ± 2.7 to –8.6 ± 4.9 mV (n = 8). In voltage-clamped HUVEC, depolarizing the holding potential from –50 to –25 mV decreased [Ca²⁺]_i significantly from 0.95 ± 0.03 to 0.88 ± 0.03 µM (n = 11, P < 0.01) and further decreased [Ca²⁺]_i to 0.47 ± 0.04 µM by depolarizing the holding potential from –25 to 0 mV (n = 11, P < 0.001). Tetraethylammonium (1 mM) inhibited EDR and the ATP-induced [Ca²⁺]_i increase in voltage-clamped MAEC. The intermediate-conductance Ca²⁺-activated K⁺ channel openers 1-ethyl-2-benzimidazolinone, chlorozoxazone, and zoxazolamine reversed the K⁺-induced inhibition of EDR and increase in [Ca²⁺]_i. The K⁺-induced inhibition of EDR and increase in [Ca²⁺]_i was abolished by the Na⁺-K⁺ pump inhibitor ouabain (10 µM). These results indicate that an increase of [K⁺]_o in the physiological range (6–12 mM) inhibits [Ca²⁺]_i increase in endothelial cells and diminishes EDR by depolarizing the membrane potential, decreasing K⁺ efflux, and activating the Na⁺-K⁺ pump, thereby modulating the release of endothelium-derived vasoactive factors from endothelial cells and vasomotor tone.

endothelial cell; intracellular calcium

This article has been cited by other articles:

				Y. Sun, M. Chen, B. H. Lowentritt, P. S. Van Zijl, K. R. Koch, S. Keay, J. M. Simard, and T. C. Chai EGF and HB-EGF modulate inward potassium current in human bladder urothelial cells from normal and interstitial cystitis patients Am J Physiol Cell Physiol, January 1, 2007; 292(1): C106 - C114. [Abstract] [Full Text] [PDF]

				M. Y. Kim, G. H. Liang, J. A. Kim, Y. J. Kim, S. Oh, and S. H. Suh Sphingosine-1-phosphate activates BKCa channels independently of G protein-coupled receptor in human endothelial cells Am J Physiol Cell Physiol, April 1, 2006; 290(4): C1000 - C1008. [Abstract] [Full Text] [PDF]

				M. Y. Kim, G. H. Seol, G. H. Liang, J. A. Kim, and S. H. Suh Na+-K+ pump activation inhibits endothelium-dependent relaxation by activating the forward mode of Na+/Ca2+ exchanger in mouse aorta Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H2020 - H2029. [Abstract] [Full Text] [PDF]