The cellular mechanisms of pacemaker-cell activity and the contribution of various ion channels of the embryonic heart are not yet fully understood. This paper presents the results of an experiment to study the effects of specific ion-channel inhibitors on the generation of action potentials in pacemaker cells of the right atrium in chicken embryos. It has been found that the exclusion of calcium ions from the extracellular solution or the strip exposure to 10 μM nifedipine (an L-type Ca2+-channel blocker) did not inhibit the generation of action potentials but led to an increase in the frequency of electrical impulses by 45%. Ryanodine, an agonist of Ca2+-channels of the sarcoplasmic reticulum, also had a positive chronotropic effect. The application of lidocaine led to a negative chronotropic effect and inhibited generation of elecrical impulses. We concluded that the role of ryanodine-sensitive Ca2+-channels (RyR-channels) of the sarcoplasmic reticulum and L-type Ca2+-channels is not crucial for maintaining the pacemaker activity in the right atrial cells of 10-day-old chicken embryos with a four-chambered heart, a not fully formed sinoatrial node, and incomplete morphofunctional maturation of the central nervous system. The demonstrated inhibition of action potential generation by lidocaine and the absence of such an effect from nifedipine indicated the substantial contribution of the Na+ current to the pacemaker activity.