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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Bondarenko, OI; Sahach, VF.
Role of mitochondria in reglulation of endothelial cell hyperpolarization to acetylcholine.
Fiziol Zh. 2006; 52(5):6-11
PubMed

 

Führende Autor*innen der Med Uni Graz
Bondarenko Oleksandr
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Abstract:
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.
Find related publications in this database (using NLM MeSH Indexing)
Acetylcholine - pharmacology
Animals -
Aorta, Thoracic - cytology Aorta, Thoracic - drug effects
Calcium - metabolism
Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology
Endothelial Cells - cytology Endothelial Cells - drug effects
Endothelium, Vascular - cytology Endothelium, Vascular - drug effects
Ionophores - pharmacology
Membrane Potentials - drug effects
Mitochondria - physiology
Rats -
Rotenone - pharmacology

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