It is well known that, in the human and other mammals, the heart rate shows an endogenous circadian rhythm over 24 h and the heart rate is lower during the sleep period than during the awake period, regardless of whether the mammal is diurnal as in the case of the human or nocturnal, for example, in the case of the mouse. This is widely attributed to the autonomic nervous system: an increase in sympathetic tone to support physical activity during the awake period and an increase in vagal tone during the sleep period (Massin et al., 2000). However, there are problems with this interpretation. For example, (i) an increase in heart rate variability at night is cited as evidence of high vagal tone (Massin et al., 2000), but we have argued that heart rate variability cannot be used to measure autonomic tone (Monfredi et al., 2014), (ii) knockout of cardiac autonomic receptors – b-receptors (1, 2 and 3) and the muscarinic M2 receptor – in the mouse is reported to have no effect on the circadian rhythm in heart rate (Swoap et al., 2008) and (iii) a circadian rhythm in heart rate is still seen in the denervated heart of heart transplant patients (Idema et al., 1994). As an alternative, we have tested the possibility that there is a circadian rhythm in the intrinsic pacemaker activity of the cardiac pacemaker, the sinus node, driven by a local circadian clock in the sinus node (Wang et al., 2016). In the mouse, there was a circadian rhythm in the heart rate in vivo in the conscious telemetrized animal, but there was also a circadian rhythm in heart rate of the isolated denervated Langendorff-perfused heart and beating rate of the isolated denervated sinus node. In the sinus node, experiments (qPCR and bioluminescence recordings in mice with a Per1 luciferase reporter) revealed functioning canonical clock genes, e.g. Bmal1 and Per1. There is, therefore, a functioning circadian clock in the sinus node. In the sinus node, we identified a circadian rhythm in the expression of some key ion channels, most notably the pacemaker channel, HCN4 (mRNA and protein measured by qPCR and western blot). HCN4 is the major isoform responsible for the funny current (If) and the density of If measured by whole cell patch clamp in isolated sinus node cells showed a prominent circadian rhythm. Block of If in the isolated sinus node by 2 mM Cs+ abolished the circadian rhythm in beating rate of the isolated sinus node. Disruption of the local circadian clock in the sinus node (by cardiac-specific knockout of Bmal1) abolished the circadian rhythm of HCN4, If density and beating rate of the isolated sinus node. Chromatin immunoprecipitation demonstrated that HCN4 is a potential transcriptional target of Bmal1 establishing a pathway by which the local clock could regulate pacemaking. In conclusion, there is a circadian rhythm in intrinsic cardiac pacemaking as a result of a local circadian clock in the sinus node that drives rhythmic expression of HCN4. The data reveal a novel regulator of cardiac pacemaking. However, the role of these intrinsic factors versus extrinsic factors, such as body temperature and even autonomic tone, has still to be determined.