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1 Department of Physiology and Medical Research Center, Ewha Women's University, College of Medicine, Seoul, Korea, Republic of
2 Department of Physiology and Medical Research Center, Ewha Women's University, College of Medicine, Seoul, Korea, Republic of; Laboratorium voor Fysiologie, Campus Gasthuisberg, Katholic University Leuven, Leuven, Belgium
3 Department of Physiology, Dankook University, College of Medicine, Chunan, Chungnam, Republic of Korea
* To whom correspondence should be addressed. E-mail: shsuh{at}ewha.ac.kr.
The effects of extracellular K+ on endothelium-dependent relaxation (EDR) and on [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 [K+]o from 6 mM to 12 mM inhibited EDR concentrationdependently. In endothelial cells (EC), an increase in [K+]o inhibited agonists-induced [Ca2+]i increase concentration-dependently. Like K+, Cs+ also inhibited EDR and [Ca2+]i increase concentration-dependently. In current-clamped HUVEC, the increase in [K+]o from 6 mM to 12 mM depolarised membrane potential from -32.8±2.7 mV to -8.6±4.9 mV (n=8). In voltage-clamped HUVEC, the depolarisation of holding potential from -50 mV to -25 mV decreased [Ca2+]i significantly from 0.95±0.03 µM to 0.88±0.03 µM (n=11; P<0.01), which was further decreased to 0.47±0.04 µM by the depolarisation from –25 mV to 0 mV (n=11; P<0.001). TEA (1 mM) inhibited EDR and 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 [Ca2+]i increase. In addition, the K+-induced inhibition of EDR and [Ca2+]i increase was abolished by the Na+-K+ pump inhibitor ouabain (10 µM). These results indicate that an increase of [K+]o in the 3 physiological range, between 6 mM to 12 mM, inhibits [Ca2+]i increase in EC and diminishes EDR by depolarising the membrane potential, by decreasing K+ efflux and by activating the Na+- K+ pump, thereby modulating the release of endothelium-derived vasoactive factors from EC and vasomotor tone.
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