Role of Adenosine A1 Receptors in Remote Ischemic Preconditioning Protection

pp 84-87

Authors

  • Diamela T. Páez Institute of Cardiovascular Physiopathology, School of Medicine, Universidad de Buenos Aires
  • Eliana P. Bin Institute of Cardiovascular Physiopathology, School of Medicine, Universidad de Buenos Aires.
  • Verónica Casanova Animal Facility, School of Veterinary Sciences, Universidad de Buenos Aires.
  • Eliana Cicale Animal Facility, School of Veterinary Sciences, Universidad de Buenos Aires.
  • Ricardo J. Gelpi Members of the National Scientific and Technical Research Council (CONICET).
  • Martín Donato Members of the National Scientific and Technical Research Council (CONICET).

DOI:

https://doi.org/10.7775/rac.es.v86.i2.12901

Keywords:

Myocardial Infarction, Receptor, Adenosine A1, Ischemic Preconditioning, Myocardial/methods, Receptor, Adenosine A3

Abstract

Background: Adenosine is involved in classical preconditioning acting especially through adenosine A1 and A3 receptors.
Objective: The objective of our study was to evaluate whether remote ischemic preconditioning (rIPC) activates adenosine A1 receptors before ischemia or at the onset of reperfusion to reduce myocardial infarct size.
Methods: Isolated rat hearts were subjected to 30-min ischemia and 60-min reperfusion (I/R). In a second group, a rIPC protocol (3 cycles of hindlimb ischemia/reperfusion) was performed. Infarct size was measured with triphenyltetrazolium staining.
Results: Remote IPC significantly decreased infarct size. This effect was abolished when DPCPX (A1 receptor blocker) or L-NAME (nitric oxide synthesis inhibitor) were administered during reperfusion.
Conclusions: We demonstrated in the isolated rat heart that rIPC reduces myocardial infarction by activation of the adenosine A1 receptor at the onset of the reperfusion period. This protective effect would be also mediated by the activation of nitric oxide synthase during reperfusion.

Published

2025-06-10

Issue

Section

ORIGINAL ARTICLES

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