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Am J Physiol Renal Physiol 282: F697-F702, 2002. First published November 13, 2001; doi:10.1152/ajprenal.00126.2001
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Vol. 282, Issue 4, F697-F702, April 2002

Role of tyrosine kinase and p44/42 MAPK in D2-like receptor-mediated stimulation of Na+, K+-ATPase in kidney

Vihang Narkar, Tahir Hussain, and Mustafa Lokhandwala

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

Our laboratory has shown that dopamine D2-like receptor activation causes stimulation of Na+, K+-ATPase (NKA) activity in the proximal tubules of the rat kidney. The present study was designed to investigate the cellular signaling mechanisms mediating this response to D2-like receptor activation. We measured the stimulation of NKA activity by bromocriptine (D2-like receptor agonist) in the absence and presence of PD-98059 [p44/42 mitogen-activated protein kinase (MAPK) kinase inhibitor] and genistein (tyrosine kinase inhibitor) in renal proximal tubules. Both agents inhibited bromocriptine-mediated stimulation of NKA, suggesting the involvement of p44/42 MAPK and tyrosine kinase in this response. Additionally, we found that bromocriptine increased the phosphorylation of p44/42 MAPK in the proximal tubules, which was blocked by PD-98059 and genistein. These results show that D2-like receptor activation causes stimulation of NKA activity by means of a tyrosine kinase-p44/42 MAPK pathway in the proximal tubules of the kidney.

dopamine; bromocriptine; proximal tubules; sodium-potassium-adenosine 5'-triphosphatase; mitogen-activated protein kinase


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