Abstract
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.
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