FCCP depolarizes plasma membrane potential by activating proton and Na+ currents in bovine aortic endothelial cells

Kyusang Park, Inho Jo, Youngmi Pak, Sung Won Bae, Hyewhon Rhim, Suk Hyo Suh, Sung Park, Mei Zhu, Insuk So, Ki Kim

Research output: Contribution to journalArticle

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Abstract

We investigated the effects of carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP), a protonophore and uncoupler of mitochondrial oxidative phosphorylation in mitochondria, on plasma membrane potential and ionic currents in bovine aortic endothelial cells (BAECs). The membrane potential and ionic currents of BAECs were recorded using the patch-clamp technique in current-clamp and voltage-clamp modes, respectively. FCCP activated ionic currents and depolarized the plasma membrane potential in a dose-dependent manner. Neither the removal of extracellular Ca2+ nor pretreatment with BAPTA/AM affected the FCCP-induced currents, implying that the currents are not associated with the FCCP-induced intracellular [Ca2+]i increase. FCCP-induced currents were significantly influenced by the changes in extracellular or intracellular pH; the increased proton gradient produced by lowering the extracellular pH or intracellular alkalinization augmented the changes in membrane potential and ionic currents caused by FCCP. FCCP-induced currents were significantly reduced under extracellular Na+-free conditions. The reversal potentials of FCCP-induced currents under Na+-free conditions were well fitted to the calculated equilibrium potential for protons. Interestingly, FCCP-induced Na+ transport (subtracted currents, Icontrol-INa+-free) was closely dependent on extracellular pH, whereas FCCP-induced H+ transport was not significantly affected by the absence of Na+. These results suggest that the FCCP-induced ionic currents and depolarization, which are strongly dependent on the plasmalemmal proton gradient, are likely to be mediated by both H+ and Na+ currents across the plasma membrane. The relationship between H+ and Na+ transport still needs to be determined.

Original languageEnglish
Pages (from-to)344-352
Number of pages9
JournalPflugers Archiv European Journal of Physiology
Volume443
Issue number3
DOIs
Publication statusPublished - 2002 Feb 5

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Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
Endothelial cells
Cell membranes
Membrane Potentials
Protons
Endothelial Cells
Cell Membrane
Induced currents
Clamping devices
Membranes
Mitochondria
Oxidative Phosphorylation
Depolarization
Patch-Clamp Techniques

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

Cite this

Park, Kyusang ; Jo, Inho ; Pak, Youngmi ; Bae, Sung Won ; Rhim, Hyewhon ; Suh, Suk Hyo ; Park, Sung ; Zhu, Mei ; So, Insuk ; Kim, Ki. / FCCP depolarizes plasma membrane potential by activating proton and Na+ currents in bovine aortic endothelial cells. In: Pflugers Archiv European Journal of Physiology. 2002 ; Vol. 443, No. 3. pp. 344-352.
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abstract = "We investigated the effects of carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP), a protonophore and uncoupler of mitochondrial oxidative phosphorylation in mitochondria, on plasma membrane potential and ionic currents in bovine aortic endothelial cells (BAECs). The membrane potential and ionic currents of BAECs were recorded using the patch-clamp technique in current-clamp and voltage-clamp modes, respectively. FCCP activated ionic currents and depolarized the plasma membrane potential in a dose-dependent manner. Neither the removal of extracellular Ca2+ nor pretreatment with BAPTA/AM affected the FCCP-induced currents, implying that the currents are not associated with the FCCP-induced intracellular [Ca2+]i increase. FCCP-induced currents were significantly influenced by the changes in extracellular or intracellular pH; the increased proton gradient produced by lowering the extracellular pH or intracellular alkalinization augmented the changes in membrane potential and ionic currents caused by FCCP. FCCP-induced currents were significantly reduced under extracellular Na+-free conditions. The reversal potentials of FCCP-induced currents under Na+-free conditions were well fitted to the calculated equilibrium potential for protons. Interestingly, FCCP-induced Na+ transport (subtracted currents, Icontrol-INa+-free) was closely dependent on extracellular pH, whereas FCCP-induced H+ transport was not significantly affected by the absence of Na+. These results suggest that the FCCP-induced ionic currents and depolarization, which are strongly dependent on the plasmalemmal proton gradient, are likely to be mediated by both H+ and Na+ currents across the plasma membrane. The relationship between H+ and Na+ transport still needs to be determined.",
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FCCP depolarizes plasma membrane potential by activating proton and Na+ currents in bovine aortic endothelial cells. / Park, Kyusang; Jo, Inho; Pak, Youngmi; Bae, Sung Won; Rhim, Hyewhon; Suh, Suk Hyo; Park, Sung; Zhu, Mei; So, Insuk; Kim, Ki.

In: Pflugers Archiv European Journal of Physiology, Vol. 443, No. 3, 05.02.2002, p. 344-352.

Research output: Contribution to journalArticle

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AU - Park, Kyusang

AU - Jo, Inho

AU - Pak, Youngmi

AU - Bae, Sung Won

AU - Rhim, Hyewhon

AU - Suh, Suk Hyo

AU - Park, Sung

AU - Zhu, Mei

AU - So, Insuk

AU - Kim, Ki

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AB - We investigated the effects of carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP), a protonophore and uncoupler of mitochondrial oxidative phosphorylation in mitochondria, on plasma membrane potential and ionic currents in bovine aortic endothelial cells (BAECs). The membrane potential and ionic currents of BAECs were recorded using the patch-clamp technique in current-clamp and voltage-clamp modes, respectively. FCCP activated ionic currents and depolarized the plasma membrane potential in a dose-dependent manner. Neither the removal of extracellular Ca2+ nor pretreatment with BAPTA/AM affected the FCCP-induced currents, implying that the currents are not associated with the FCCP-induced intracellular [Ca2+]i increase. FCCP-induced currents were significantly influenced by the changes in extracellular or intracellular pH; the increased proton gradient produced by lowering the extracellular pH or intracellular alkalinization augmented the changes in membrane potential and ionic currents caused by FCCP. FCCP-induced currents were significantly reduced under extracellular Na+-free conditions. The reversal potentials of FCCP-induced currents under Na+-free conditions were well fitted to the calculated equilibrium potential for protons. Interestingly, FCCP-induced Na+ transport (subtracted currents, Icontrol-INa+-free) was closely dependent on extracellular pH, whereas FCCP-induced H+ transport was not significantly affected by the absence of Na+. These results suggest that the FCCP-induced ionic currents and depolarization, which are strongly dependent on the plasmalemmal proton gradient, are likely to be mediated by both H+ and Na+ currents across the plasma membrane. The relationship between H+ and Na+ transport still needs to be determined.

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