Key result
Adenosine A2A receptor stimulation affected only the fast time constant for I Ca inactivation, suggesting a PKA-mediated increase in ryanodine receptor opening.
This reply clarifies the proposed mechanism by which adenosine A2A receptor stimulation increases calcium sparks in human atrial myocytes via PKA-mediated ryanodine receptor opening.
In our paper on the expression and function of the adenosine A2A receptor (A2AR) in human atrial myocytes [1], we show that agonist stimulation of this receptor induces a protein kinase A (PKA)-dependent increase in the frequency of calcium sparks and spontaneous calcium waves. We therefore investigated whether A2AR stimulation affected the L-type calcium current, sarcoplasmic reticulum (SR) calcium uptake, or SR calcium release, as these mechanisms are known to be modulated by PKA-dependent phosphorylation [2–4]. Since only the fast (SR calcium release-dependent) time constant for I Ca inactivation was affected by A2AR stimulation, we proposed that a PKA-mediated increase in ryanodine receptor (RyR) opening may account for our results. However, according to the letter …
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Hove‐Madsen et al. (2006) reported a letter. Adenosine A2A receptor (A2AR) stimulation was evaluated on L-type calcium current, sarcoplasmic reticulum (SR) calcium uptake, or SR calcium release. Adenosine A2A receptor stimulation affected only the fast time constant for I Ca inactivation, suggesting a PKA-mediated increase in ryanodine receptor opening.
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