Pacemaker activity of sino-atrial myocytes permanently controls the heart rate. Heart automaticity is modulated by the autonomic nervous system, which regulates the activity of ion channels of the plasma membrane in automatic cells. Several classes of ion channels contribute to pacemaking. The functional role of voltage-dependent calcium channels (VGCCs) in heart automaticity and impulse conduction has been matter of debate for 30 years. Here we present and discuss recent evidence showing that VGCCs are important mechanisms underlying pacemaker activity and impulse conduction. Indeed, studies performed in genetically modified mice lacking L-type Cav1.3 (Cav1.3−/−) or T-type Cav3.1 (Cav3.1−/−) channels demonstrate that ablation of these channels severely impairs pacemaker activity. In sino-atrial myocytes, VGCCs activate at negative voltages at the beginning of the diastolic depolarization and importantly contribute to this phase by supplying inward current. Ablation or loss-of-function of these channels induces also heart block. Furthermore, inactivation of Cav1.3 channels promotes also tachy-brady syndromes in knockout mice indicating that these channels are important in stabilisation of atrial rhythm. Genomic analysis demonstrated that Cav1.3 and Cav3.1 channels are widely expressed in pacemaker tissue of mice, rabbits and humans. Importantly, human diseases of automaticity such as congenital bradycardia and heart block have been attributed to loss-of-function of Cav1.3 and Cav3.1 channels.