Profound regulation of Na/K pump activity by transient elevations of cytoplasmic calcium in murine cardiac myocytes

Fang Min Lu, Christine Deisl, Donald W. Hilgemann

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Small changes of Na/K pump activity regulate internal Ca release in cardiac myocytes via Na/Ca exchange. We now show conversely that transient elevations of cytoplasmic Ca strongly regulate cardiac Na/K pumps. When cytoplasmic Na is submaximal, Na/K pump currents decay rapidly during extracellular K application and multiple results suggest that an inactivation mechanism is involved. Brief activation of Ca influx by reverse Na/Ca exchange enhances pump currents and attenuates current decay, while repeated Ca elevations suppress pump currents. Pump current enhancement reverses over 3 min, and results are similar in myocytes lacking the regulatory protein, phospholemman. Classical signaling mechanisms, including Ca-activated protein kinases and reactive oxygen, are evidently not involved. Electrogenic signals mediated by intramembrane movement of hydrophobic ions, such as hexyltriphenylphosphonium (C6TPP), increase and decrease in parallel with pump currents. Thus, transient Ca elevation and Na/K pump inactivation cause opposing sarcolemma changes that may affect diverse membrane processes.

Original languageEnglish (US)
Article numbere19267
JournaleLife
Volume5
DOIs
StatePublished - 2016

ASJC Scopus subject areas

  • General Neuroscience
  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology

Fingerprint

Dive into the research topics of 'Profound regulation of Na/K pump activity by transient elevations of cytoplasmic calcium in murine cardiac myocytes'. Together they form a unique fingerprint.

Cite this