Hydrogen peroxide, potassium currents, and membrane potential in human endothelial cells

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Item Type:	Article
Title:	Hydrogen peroxide, potassium currents, and membrane potential in human endothelial cells
Creators Name:	Bychkov, R., Pieper, K., Ried, C., Milosheva, M., Bychkov, E., Luft, F.C. and Haller, H.
Abstract:	BACKGROUND: Hydrogen peroxide (H2O2) and reactive oxygen species are implicated in inflammation, ischemia-reperfusion injury, and atherosclerosis. The role of ion channels has not been previously explored. METHODS AND RESULTS: K+ currents and membrane potential were recorded in endothelial cells by voltage- and current-clamp techniques. H2O2 elicited both hyperpolarization and depolarization of the membrane potential in a concentration-dependent manner. Low H2O2 concentrations (0.01 to 0.25 micromol/L) inhibited the inward-rectifying K+ current (KIR). Whole-cell K+ current analysis revealed that H2O2 (1 mmol/L) applied to the bath solution increased the Ca2+-dependent K+ current (KCa) amplitude. H2O2 increased KCa current in outside-out patches in a Ca2+-free solution. When catalase (5000 micro/mL) was added to the bath solution, the outward-rectifying K+ current amplitude was restored. In contrast, superoxide dismutase (1000 u/mL) had only a small effect on the H2O2-induced K+ current changes. Next, we measured whole-cell K+ currents and redox potentials simultaneously with a novel redox potential-sensitive electrode. The H2O2-mediated KCa current increase was accompanied by a whole-cell redox potential decrease. CONCLUSIONS: H2O2 elicited both hyperpolarization and depolarization of the membrane potential through 2 different mechanisms. Low H2O2 concentrations inhibited inward-rectifying K+ currents, whereas higher H2O2 concentrations increased the amplitude of the outward K+ current. We suggest that reactive oxygen species generated locally increases the KCa current amplitude, whereas low H2O2 concentrations inhibit KIR via intracellular messengers.
Keywords:	Nitric Oxide, Potassium, Free Radicals, Endothelium
Source:	Circulation
ISSN:	0009-7322
Publisher:	American Heart Association
Volume:	99
Number:	13
Page Range:	1719-1725
Date:	6 April 1999
Official Publication:	http://circ.ahajournals.org/cgi/content/abstract/99/13/1719
PubMed:	View item in PubMed

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