| Autor: |
Budu, Claudia E., Efendiev, Riad, Cinelli, Angel M., Bertorello, Alejandro M., Pedemonte, Carlos H. |
| Předmět: |
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| Zdroj: |
British Journal of Pharmacology; Dec2002, Vol. 137 Issue 8, p1380-1386, 7p |
| Abstrakt: |
1 The present study demonstrates that stimulation of hormonal receptors of proximal tubule cells with the serotonin-agonist 8-hydroxy-2-(di-n-propylamino) tetraline (8-OH-DPAT) induces an augmentation of Na[SUP+], K[SUP+]-ATPase activity that results from the recruitment of enzyme molecules to the plasmalemma. 2 Cells expressing the rodent wild-type Na[SUP+], K[SUP+]-ATPase α-subunit had the same basal Na[SUP+], K[SUP+]-ATPase activity as cells expressing the α-subunit S11A S18A mutants, but stimulation of Na[SUP+], K[SUP+]-ATPase activity was completely abolished in either mutant. 3 8-OH-DPAT treatment of OK cells led to PKC-dependent phosphorylation of the α-subunit Ser-11 and Ser-18 residues, and determination of enzyme activity with the S11A and S18A mutants indicated that both residues are essential for the agonist-dependent stimulation of Na[SUP+], K[SUP+]-ATPase activity. 4 When cells were treated with both dopamine and 8-OH-DPAT, and activation of Na[SUP+], K[SUP+]-ATPase was observed at basal intracellular sodium concentration (∼9 mM), and this activation was gradually reduced and became a significant inhibition as the concentration of intracellular sodium gradually increased from 9 to 19 mM. Thus, besides the antagonistic effects of dopamine and 8-OH-DPAT, intracellular sodium modulates whether an activation or an inhibition of Na[SUP+], K[SUP+]-ATPase is produced. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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