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Reduced Basal Heart Rate Variability in a Calcineurin Aβ Deficient Mouse

Heart rate and heart rhythm, quantified by heart rate variability (HRV) in vivo, are both determined by intrinsic pacemaker activity of sinoatrial node (SAN) pacemaker cells (SANC), and input to SAN from the autonomic nervous system (ANS). The spontaneous action potential (AP) firing rate and rhythm of SANC are governed, at least in part, by phosphorylation of proteins that regulate their intracellular calcium cycling and ion channel functions. Calcineurin Aβ (CnAβ), the catalytic subunit of a calcium‐activated serine/threonine phosphatase, influences SANC function protein phosphorylation. Increased calcium cycling and ion channel phosphorylation leads to an increase in SANC AP firing rate and reduced AP firing interval variability. CnAβ likely impacts SANC AP firing rate and AP interval variability, making CnAβ a prime candidate of in vivo HR and HRV regulation. Thus, we hypothesized the role of CnAβ in CnAβ−/− mice, in which cardiac Cn activity is decreased by 80%, would manifest an increased in vivo HR and reduced HRV.