Activation of D2-like receptors causes recruitment of tyrosine-phosphorylated NKA alpha 1-subunits in kidney.
Activation of D2-like receptors causes recruitment of tyrosine-phosphorylated NKA alpha 1-subunits in kidney.
复制标题
D2 样受体的激活导致肾脏中酪氨酸磷酸化的 NKA α 1 亚基的募集。
DOI：
10.1152/ajprenal.00039.2002
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Lokhandwala,MustafaF
中科院分区：
文献类型：
--
作者：
Narkar,VihangA;Hussain,Tahir;Lokhandwala,MustafaF
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 α1-subunits of the enzyme from cytosol to the membrane. This hypothesis was tested by Western blotting for Na+-K+-ATPase α1-subunits in proximal tubular membrane. Treatment of the proximal tubules with bromocriptine (D2-like receptor agonist) caused an increase in Na+-K+-ATPase α1-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 α1-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 α1-subunits. In conclusion, we have demonstrated that activation of D2-like receptors increases Na+-K+-ATPase activity by recruitment of the tyrosine-phosphorylated α1-subunits in the proximal tubules of the kidney.
