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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

Inhibition of the voltage-dependent calcium current by extracellular ATP in hamster ventricular cardiomyocytes

F Von zur Mühlen1, B D Gonska, H Kreuzer

  • 1Department of Cardiology, University of Göttingen, Germany.

The American Journal of Physiology
|July 1, 1997
PubMed

Insights

External ATP inhibits high-voltage-activated calcium current (ICa) in hamster heart cells. This effect occurs via P2 purinergic receptors and may be relevant in myocardial injury.

Area of Science:

  • Cardiovascular Physiology
  • Cellular Electrophysiology
  • Purinergic Signaling

Background:

  • High-voltage-activated calcium current (ICa) is crucial for cardiac function.
  • Extracellular ATP's role in modulating cardiac ion channels is not fully understood.
  • Purinergic receptors are involved in various physiological and pathophysiological processes.

Purpose of the Study:

  • To investigate the effect of external ATP on ICa in hamster ventricular cardiomyocytes.
  • To elucidate the mechanism and receptor subtype involved in ATP-mediated ICa modulation.
  • To assess the potential pathophysiological relevance of this interaction.

Main Methods:

  • Whole-cell patch-clamp technique applied to single hamster ventricular myocytes.
  • Extracellular application of ATP and its analogs (0.1-100 microM).
  • Assessment of ICa inhibition, time course, current-voltage relationships, and involvement of intracellular signaling molecules.

Main Results:

  • Extracellular ATP reversibly inhibited ICa by up to 30% with slow kinetics.
  • The inhibition was mediated by a P2 purinergic receptor, as indicated by analog potency and lack of P1 receptor antagonist effect.
  • Internal GTPγS suggested involvement of a G protein not coupled to adenylate cyclase, while cAMP levels had no effect.

Conclusions:

  • External ATP inhibits ICa in hamster ventricular myocytes through a P2 purinergic receptor.
  • The mechanism involves a G protein signaling pathway distinct from adenylate cyclase activation.
  • This extracellular ATP-induced ICa inhibition may have implications in myocardial injury scenarios.

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