Different Mechanisms of Renal Na-K-ATPase Regulation by Dopamine in the Proximal and Distal Nephron

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    • SATOH Takeo
    • First Department of Internal Medicine, St. Mariannna University School of Medicine
    • OMINATO Masayuki
    • First Department of Internal Medicine, St. Mariannna University School of Medicine
    • KATZ Adrian I.
    • Department of Medicine, University of Chicago Pritzker School of Medicine


We reported a novel intracellular mechanism of renal Na-K-ATPase regulation by dopamine (DA) in the rat cortical collecting duct (CCD), which involves stimulation of protein kinase A (PKA) and phospholipase A<sub>2</sub> (PLA<sub>2</sub>). In the present experiments we determined whether this mechanism also operates in other nephron segments. In the medullary thick ascending limbs (MTAL), DA and other cAMP agonists inhibited Na-K-ATPase activity, an effect that was abolished by PKA inhibitor IP<sub>20</sub>, but various protein kinase C (PKC) activators did not, analogous to our previous findings in CCD. In sharp contrast, DA inhibition on Na-K-ATPase in the proximal convoluted tubule (PCT) was reproduced by PKC agonists. These effects was blocked by PKC inhibitor staurosporine, but not by IP<sub>20</sub>. Mepacrine, a PLA<sub>2</sub> inhibitor, reversed the pump effect of all agents, and arachidonic acid (AA) produced a dose-dependent pump inhibition, in all three nephron segments.<br>We conclude that the intercellular mechanisms of Na-K-ATPase regulation by dopamine differ in the proximal and distal nephron, as they involve stimulation of PKA in MTAL and CCD, and of PKC in PCT. These two pathways probably share a common mechanism in stimulating PLA<sub>2</sub> and AA release in both regions of the nephron. (<i>Hypertens Res</i> 1995; 18 Suppl. I: S137-S140)


  • Hypertension Research

    Hypertension Research 18, S137-S140, 1995-06-01

    The Japanese Society of Hypertension


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