[Role of mitochondria in reglulation of endothelial cell hyperpolarization to acetylcholine].
We investigated the regulation of sustained endothelial hyperpolarization to acetylcholine in the rat aortic endothelial cells by mitochondria. Protonofore CCCP and rotenone, an electron transport chain complex I inhibitor, agents that cause mitochondria depolarization, inhibited the sustained hyperpolarization of endothelial cells. This effect was unlikely to be mediated by the free radicals since hydrogen peroxide was shown to hyperpolarize endothelial cells. It is concluded that mitochondrial Ca2+ uptake is essential in prolongation of endothelial hyperpolarization to acetylcholine.
Bondarenko
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OI
Sahach
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VF
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone / Q000494:pharmacology; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects*; D066298:In Vitro Techniques; D007476:Ionophores / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects*; D008928:Mitochondria / Q000502:physiology*; D051381:Rats; D012402:Rotenone / Q000494:pharmacology
D007476:Ionophores; D012402:Rotenone; D002258:Carbonyl Cyanide m-Chlorophenyl Hydrazone; D000109:Acetylcholine; D002118:Calcium