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Am J Physiol Renal Physiol 283: F1290-F1295, 2002. First published July 30, 2002; doi:10.1152/ajprenal.00039.2002
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Vol. 283, Issue 6, F1290-F1295, December 2002

Activation of D2-like receptors causes recruitment of tyrosine-phosphorylated NKA alpha 1-subunits in kidney

Vihang A. Narkar, Tahir Hussain, and Mustafa F. Lokhandwala

Institute for Cardiovascular Studies, College of Pharmacy, University of Houston, Houston, Texas 77204-5515

The present study investigates the cellular mechanisms responsible for dopamine D2-like receptor-mediated stimulation of Na+-K+-ATPase in the proximal tubules of the kidney. Previously, we showed that D2-like receptor-mediated increase in Na+-K+-ATPase involves an increase in the maximum rate of Na+-K+-ATPase activity (Vmax). Therefore, we tested the hypothesis that D2-like receptor-mediated stimulation of Na+-K+-ATPase requires phosphorylation and recruitment of alpha 1-subunits of the enzyme from cytosol to the membrane. This hypothesis was tested by Western blotting for Na+-K+-ATPase alpha 1-subunits in proximal tubular membrane. Treatment of the proximal tubules with bromocriptine (D2-like receptor agonist) caused an increase in Na+-K+-ATPase alpha 1-subunit abundance in the membrane preparations. This effect was blocked by genistein (tyrosine kinase inhibitor), suggesting a role for tyrosine phosphorylation. Moreover, bromocriptine caused an increase in tyrosine phosphorylation of membrane-bound Na+-K+-ATPase alpha 1-subunits. This effect was blocked by bafilomycin A1 (vesicular trafficking inhibitor), which suggested that this increase was due to the recruitment of tyrosine-phosphorylated Na+-K+-ATPase alpha 1-subunits. In conclusion, we have demonstrated that activation of D2-like receptors increases Na+-K+-ATPase activity by recruitment of the tyrosine-phosphorylated alpha 1-subunits in the proximal tubules of the kidney.

dopamine; bromocriptine; bafilomycin A1; genistein; proximal tubules; sodium/potassium/adenosine 5'-triphosphatase


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