Adenosine A2A receptors are expressed in human atrial myocytes and modulate spontaneous sarcoplasmic reticulum

Leif Hove-Madsen1, Cristina Prat-Vidal, Anna Llach

  • 1Cell Physiology Laboratory, Cardiology Department, Hospital de la Santa Creu i Sant Pau, Institut Catalá de Ciencies Cardiovasculars, Universitat Autònoma de Barcelona, St Antoni M(a) Claret 167, 08025 Barcelona, Spain. lhove@santpau.es

Cardiovascular Research
|October 4, 2006
PubMed
Abstract

Insights

Adenosine A(2A) receptors are present in human heart cells and influence spontaneous calcium release. This finding is crucial for understanding heart rhythm disorders like atrial fibrillation.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Altered cyclic AMP regulation of cardiac ryanodine receptors (RyR2) is linked to spontaneous calcium release in heart failure and arrhythmias.
  • The role of adenosine A(2A) receptors (A(2A)R) in regulating cyclic AMP and their presence in human cardiac myocytes were previously uninvestigated.

Purpose of the Study:

  • To determine the expression and function of adenosine A(2A) receptors in human cardiac myocytes.
  • To investigate the impact of A(2A)R stimulation on calcium handling in the human atrium.

Main Methods:

  • Utilized PCR, western blotting, and immunofluorescence to detect A(2A)R expression.
  • Employed confocal calcium imaging and patch-clamp techniques to assess functional effects of A(2A)R stimulation.

Main Results:

  • A(2A)R expression was confirmed in the human right atrium, co-localizing with RyR2.
  • A(2A)R stimulation significantly increased spontaneous calcium release, calcium sparks, calcium waves, and spontaneous Na-Ca exchange currents (I(NCX)) in atrial myocytes.
  • No significant alterations were observed in caffeine-inducible calcium release or L-type calcium current amplitude, though calcium release-dependent inactivation was accelerated.

Conclusions:

  • Adenosine A(2A) receptors are expressed in the human atrial myocardium.
  • A(2A)R activation modulates the frequency of spontaneous calcium release from the sarcoplasmic reticulum, offering potential therapeutic targets for cardiac arrhythmias.

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