Abstract
Constitutive cAMP-PKA signaling to sarcoplasmic reticulum (SR) in sinoatrial nodal cells (SANC) generates spontaneous, rhythmic local Ca2+ releases (LCRs) beneath the surface membrane, that underlie the Action Potential (AP) Intrinsic Firing Rate (IAPFR). IAPFR in vivo, and in isolated sinoatrial nodes (SAN) declines between 2-4 and 22-24 months in C57 black mice and augmentation of AP firing rate in response to phophodiesterase (PDE) inhibition, which prevents cAMP degradation and augments PKA-dependent phosphorylation of SR Ca2+ cycling proteins, declines with age.
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