Regulation of Na+,K(+)-ATPase activity by dopamine in cultured rat aortic smooth muscle cells.
Regulation of Na+,K(+)-ATPase activity by dopamine in cultured rat aortic smooth muscle cells.
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DOI：
10.1016/0014-2999(96)00179-3
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发表时间：
1996-06
影响因子：
5
通讯作者：
S. Rashed;E. Songu‐Mize
中科院分区：
文献类型：
--
作者：
S. Rashed;E. Songu‐Mize
We investigated the effect of dopamine on Na+,K+-ATPase activity in cultured aortic smooth muscle cells. Na+,K+-ATPase activity was measured by a coupled enzyme assay. Our results demonstrate that dopamine and dopamine receptor agonists, SKF-38393 (a D1receptor agonist) and quinpirole (a D2receptor agonist) produced 62%, 50% and 49% inhibition of Na+,K+-ATPase activity in aortic smooth muscle cells, respectively. The combination of the two agonists produced inhibition similar to that of dopamine. Dopamine- and the agonist-induced Na+,K+-ATPase inhibition was blocked by selective receptor antagonists. The Na+,K+-ATPase inhibition by SKF-38393 but not by quinpirole was abolished by pertussis toxin. Na+,K+-ATPase inhibition was also achieved by guanosine triphosphate analog GTP-γ-S. SKF-38393 but not quinpirole stimulated phosphoinositide hydrolysis rate in rat aortic slices. SKF-38393-induced phosphoinositide hydrolysis stimulation was reversed by SCH-23390, a dopamine D1receptor antagonist, and attenuated by pertussis toxin. In conclusion, our observations indicate that dopamine and dopamine receptor agonists inhibit Na+,K+-ATPase activity through specific vascular receptors. Dopamine D1receptors are linked to pertussis toxin sensitive-mechanism(s) and a GTP-binding protein appears to be coupled to the enzyme inhibition. Finally, the inhibition of Na+,K+-ATPase activity in response to dopamine D1receptor activation may be mediated by the phospholipase C signaling pathway.
