Angiotensin regulates the selectivity of the Na+-K+ pump for intracellular Na+

Kerrie A. Buhagiar, Peter S. Hansen, David F. Gray, Anastasia S. Mihailidou, Helge H. Rasmussen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

31 Citations (Scopus)

Abstract

Treatment of rabbits with angiotensin-converting enzyme (ACE) inhibitors increases the apparent affinity of the Na+-K+ pump for Na+. To explore the mechanism, we voltage clamped myocytes from control rabbits and rabbits treated with captopril with patch pipettes containing 10 mM Na+. When pipette solutions were K+ free, pump current (I(p)) for myocytes from captopril-treated rabbits was nearly identical to that for myocytes from controls. However, treatment caused a significant increase in I(p) measured with pipettes containing K+. A similar difference was observed when myocytes from rabbits treated with the ANG II receptor antagonist losartan and myocytes from controls were compared. Treatment-induced differences in I(p) were eliminated by in vitro exposure to ANG II or phorbol 12-myristate 13- acetate or inclusion of the protein kinase C fragment composed of amino acids 530-558 in pipette solutions. Treatment with captopril had no effect on the voltage dependence of I(p). We conclude that ANG II regulates the pump's selectivity for intracellular Na+ at sites near the cytoplasmic surface. Protein kinase C is implicated in the messenger cascade.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Volume277
Issue number3 46-3
Publication statusPublished - 1999
Externally publishedYes

Keywords

  • Cardiac myocytes
  • Protein kinase C
  • Sodium

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