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Involvement of reactive oxygen species in Kv channels inhibition induced by hypoxia in rat pulmonary arteries
Author(s) -
Frazziano Giovanna,
Cogolludo Angel,
Moreno Laura,
Lodi Federica,
Cobeño Laura,
Tamargo Juan,
PerezVizcaino Francisco
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1171-d
Subject(s) - apocynin , rotenone , reactive oxygen species , mesenteric arteries , dichlorofluorescein , hypoxic pulmonary vasoconstriction , hypoxia (environmental) , chemistry , tiron , mitochondrial ros , catalase , superoxide , nadph oxidase , pharmacology , biophysics , oxygen , biochemistry , medicine , pulmonary artery , mitochondrion , biology , oxidative stress , artery , enzyme , organic chemistry
The objective of this study was to analyse the possible role of an increased production of reactive oxygen species (ROS) in hypoxia‐induced inhibition of Kv currents in rat pulmonary arteries. We found that hypoxia induced an increase in ROS, measured by the fluorescence of dichlorofluorescein and dihydroethidium (indicators of intracellular H 2 0 2 and O 2 − respectively). Increase in DFC fluorescence was prevented by the NADPH inhibitor apocynin and the mitochondrial respiratory chain inhibitor rotenone. In addition, the increase in DHE fluorescence was inhibited by the superoxide scavenger tiron. Hypoxia inhibited Kv currents and this effect was markedly prevented by apocynin, rotenone and catalase. Furthermore, the membrane permeable form of hydroperoxide, t‐butyl hydroperoxide, inhibited Kv currents and contracted pulmonary arteries but not mesenteric arteries. Our results suggest that an increase in ROS are involved in hypoxia–induced inhibition of Kv currents in pulmonary arteries Supported by AGL2004‐06685/ALI and SAF2005‐03770