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Reactive oxygen species mediate dopamine‐induced signaling in renal proximal tubule cells
Author(s) -
Acquier Andrea B.,
Mori Sequeiros García Mercedes,
Gorostizaga Alejandra B.,
Paz Cristina,
Mendez Carlos F.
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.08.020
Subject(s) - reactive oxygen species , chemistry , reabsorption , renal sodium reabsorption , dopamine , superoxide dismutase , microbiology and biotechnology , mitochondrion , superoxide , sodium , medicine , endocrinology , mitochondrial ros , signal transduction , kidney , oxidative stress , biochemistry , biology , enzyme , organic chemistry
Intrarenally‐produced dopamine (DA) induces a large increase in urinary sodium excretion mainly due to the inhibition of tubular sodium reabsorption. We aimed to study the participation of reactive oxygen species (ROS) in DA signaling pathway in proximal tubule cells. Our results show that DA increased ROS production in OK cells and indicate the mitochondria as the main source of ROS. DA also increased ERK1/2, superoxide dismutase (SOD) and transcription factor κB (NF‐κB) activity. These findings suggest that DA generates mitochondria‐derived ROS that activate ERK1/2 and subsequently NF‐κB and SOD activity at concentrations that exert a physiological regulation of renal function.