Dopamine D₅ receptor-mediated decreases in mitochondrial reactive oxygen species production are cAMP and autophagy dependent.

ABSTRACT: Overproduction of reactive oxygen species (ROS) plays an important role in the pathogenesis of hypertension. The dopamine D₅ receptor (D₅R) is known to decrease ROS production, but the mechanism is not completely understood. In HEK293 cells overexpressing D₅R, fenoldopam, an agonist of the two D₁-like receptors, D₁R and D₅R, decreased the production of mitochondria-derived ROS (mito-ROS). The fenoldopam-mediated decrease in mito-ROS production was mimicked by Sp-cAMPS but blocked by Rp-cAMPS. In human renal proximal tubule cells with DRD1 gene silencing to eliminate the confounding effect of D₁R, fenoldopam still decreased mito-ROS production. By contrast, Sch23390, a D₁R and D₅R antagonist,

SUBMITTER: Lee H 

PROVIDER: S-EPMC8369611 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature