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• W2018201418 abstract "Modulation of Ca2+-activated K+ channel in renal artery endothelium in situ by nitric oxide and reactive oxygen species.BackgroundEndothelium-derived nitric oxide and reactive oxygen species (ROS) have been proposed to regulate vascular tone by complex mechanisms, including the modulation of ion channel function. In endothelial function itself, activation of Ca2+-activated K+ channels (KCa) plays a crucial role by inducing hyperpolarization, which promotes membrane potential-driven Ca2+ influx and Ca2+-dependent synthesis of vasodilatory factors. In the present study, we tested whether nitric oxide and ROS modulate endothelial KCa function.MethodsBy employing the patch-clamp technique in endothelium of porcine renal arteries in situ, we identified a large-conductance Ca2+-activated K+ channel (big K+ channel, BKCa) with a conductance of 297 ± 6 pS.ResultsChannel activity was strongly controlled by the membrane potential and the cytosolic Ca2+ concentration (EC50 3.1 ± 0.5 μmol/L Ca2+ at 0 mV). Channel activity was inhibited by Ba2+ and iberiotoxin. At submicromolar [Ca2+]i, nitric oxide induced a dose-dependent stimulation of BKCa activity with a 10-fold increase at the highest dose tested (1 μmol/L). A similar stimulation was achieved by the nitric oxide donors, sodium nitroprusside (SNP), and diethylamine nitric oxide complex (DEA-NO). In contrast, ROS and, in particular, hydrogen peroxide (H2O2) led to dose-dependent inactivation of BKCa with an IC50 of 80 ± 6 nmol/L and 1.1 ± 0.4 μmol/L, respectively. In isolated porcine renal arteries, bradykinin-induced vasodilation was significantly reduced by either iberiotoxin or H2O2.ConclusionDirect stimulation of endothelial BKCa by nitric oxide might represent a novel mechanism of autocrine regulation of endothelial function and points to a positive feedback mechanism by promoting hyperpolarization and nitric oxide production itself. The ROS-induced inhibition of BKCa could be part of the cellular mechanisms by which ROS impairs endothelium-dependent vasodilation. Modulation of Ca2+-activated K+ channel in renal artery endothelium in situ by nitric oxide and reactive oxygen species. Endothelium-derived nitric oxide and reactive oxygen species (ROS) have been proposed to regulate vascular tone by complex mechanisms, including the modulation of ion channel function. In endothelial function itself, activation of Ca2+-activated K+ channels (KCa) plays a crucial role by inducing hyperpolarization, which promotes membrane potential-driven Ca2+ influx and Ca2+-dependent synthesis of vasodilatory factors. In the present study, we tested whether nitric oxide and ROS modulate endothelial KCa function. By employing the patch-clamp technique in endothelium of porcine renal arteries in situ, we identified a large-conductance Ca2+-activated K+ channel (big K+ channel, BKCa) with a conductance of 297 ± 6 pS. Channel activity was strongly controlled by the membrane potential and the cytosolic Ca2+ concentration (EC50 3.1 ± 0.5 μmol/L Ca2+ at 0 mV). Channel activity was inhibited by Ba2+ and iberiotoxin. At submicromolar [Ca2+]i, nitric oxide induced a dose-dependent stimulation of BKCa activity with a 10-fold increase at the highest dose tested (1 μmol/L). A similar stimulation was achieved by the nitric oxide donors, sodium nitroprusside (SNP), and diethylamine nitric oxide complex (DEA-NO). In contrast, ROS and, in particular, hydrogen peroxide (H2O2) led to dose-dependent inactivation of BKCa with an IC50 of 80 ± 6 nmol/L and 1.1 ± 0.4 μmol/L, respectively. In isolated porcine renal arteries, bradykinin-induced vasodilation was significantly reduced by either iberiotoxin or H2O2. Direct stimulation of endothelial BKCa by nitric oxide might represent a novel mechanism of autocrine regulation of endothelial function and points to a positive feedback mechanism by promoting hyperpolarization and nitric oxide production itself. The ROS-induced inhibition of BKCa could be part of the cellular mechanisms by which ROS impairs endothelium-dependent vasodilation." @default.
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• W2018201418 date "2003-07-01" @default.
• W2018201418 modified "2023-10-15" @default.
• W2018201418 title "Modulation of Ca2+-activated K+ channel in renal artery endothelium in situ by nitric oxide and reactive oxygen species" @default.
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• W2018201418 doi "https://doi.org/10.1046/j.1523-1755.2003.00051.x" @default.
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