We have shown recently that the intrinsic heart rate (IHR) in vivo (measured during double autonomic blockade) in mice with cardiac-specific overexpression of adenylyl cyclase type VIII(AC VIII) is 30% higher than in wild type littermates (WT). We studied single sinoatrial nodal cell (SANC)to elucidate how AC VIII overexpression affects a coupled-clock system that drives spontaneous action potential (AP) firing in these cells. Spontaneous local Ca2+ releases (LCRs, confocal line-scan microscopy), generated via spontaneous local activation of ryanodine receptors (RyR) of the intracellular Ca2+ oscillator-sarcoplasmic reticulum (SR), occurred earlier in diastole in TgAC8 SANC, accelerating the diastolic AP ignition process that governs the rate of spontaneous diastolic depolarization. This led to an increased rate of AP generation by the ensemble of cell surface membrane ionic current oscillators. In permeabilized (saponin) SANC, Ca2+ signal of individual LCR's, and that of the LCR ensemble were increased in TgAC8 vs WT. Double immunostaining of phosphorylated and total RyR revealed increased phosphorylation of RyR at Ser2808 and Ser2030, and of PLB at Ser16 sites in TgAC8 vs WT SANC. RNA-seq analysis showed an upregulation of several PDEs (including PDE1a, PDE3a, PDE4b, PDE4c, PDE4d, PDE7b and PDE8a), ion channels (Cacna1c, Cacnb2, Kcnb1, Kcnd3, Kcnn1, Kcnq1, Scn1b, Scn4a; Kcnj3 however was downregulated), ATPase Na+/K+ transporters (ATP1a1 and ATP2b1) and calcium cycling proteins (STIM1 and RYR2) were upregulated in TgAC8 vs WT (notably, SIN and PLM were downregulated in TgAC8 vs WT). Thus, cardiac-specific overexpression of AC VIII in SANC increases IHR in vivo via impacting upon both transcriptional and posttranslational proteins modification of the Ca2+-cAMP-PKA-dependent components of the coupled-oscillator system intrinsic to SANC that controls their spontaneous AP firing rate.