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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
10:53

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents

Published on: July 3, 2013

Control of the cardiac muscarinic K+ channel by beta-arrestin 2

Z Shui1, I A Khan, T Haga

  • 1School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom.

The Journal of Biological Chemistry
|January 22, 2001
PubMed

Insights

Beta-arrestin 2 significantly enhances desensitization of the cardiac muscarinic K(+) current (i(K,ACh)) and slows its resensitization. This protein plays a key role in regulating i(K,ACh) function.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Signaling

Background:

  • The cardiac muscarinic K(+) current (i(K,ACh)) is crucial for regulating heart rate.
  • Beta-arrestin 2 is known to be involved in G protein-coupled receptor desensitization.

Purpose of the Study:

  • To investigate the role of beta-arrestin 2 in the control of cardiac muscarinic K(+) current (i(K,ACh)).

Main Methods:

  • Chinese hamster ovary (CHO) cells were transfected with m2 muscarinic receptors, muscarinic K(+) channels, GRK2, and beta-arrestin 2.
  • Electrophysiological recordings were used to measure i(K,ACh) desensitization, resensitization, activation, and deactivation.

Main Results:

  • Beta-arrestin 2 significantly increased i(K,ACh) desensitization (45% to 78%) and slowed resensitization (time constant from 34 to 232 s).
  • Activation and deactivation kinetics of i(K,ACh) were significantly slowed by beta-arrestin 2.
  • A constitutively active beta-arrestin 2 mutant induced desensitization even without agonist stimulation.

Conclusions:

  • Beta-arrestin 2 plays a major role in the desensitization of the cardiac muscarinic K(+) channel.
  • Beta-arrestin 2 influences other functional aspects of the muscarinic K(+) channel, including activation and deactivation kinetics.

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