Aim Spontaneous activity of embryonic cardiomyocytes originates from sarcoplasmic reticulum (SR) Ca2+ release during early cardiogenesis. However, the regulation of heart rate during embryonic development is still not clear. The aim of this study was to determine how endothelin‐1 (ET‐1) affects the heart rate of embryonic mice, as well as the pathway through which it exerts its effects. Methods The effects of ET‐1 and ET‐1 receptor inhibition on cardiac contraction were studied using confocal Ca2+ imaging of isolated mouse embryonic ventricular cardiomyocytes and ultrasonographic examination of embryonic cardiac contractions in utero. In addition, the amount of ET‐1 and ET receptor a (ETa) and b (ETb) mRNA levels during different stages of development of the cardiac muscle was measured. Results High ET‐1 concentration and expression of both ETa‐ and ETb‐receptors was observed in early cardiac tissue. ET‐1 was found to increase the frequency of spontaneous Ca2+ oscillations in E10.5 embryonic cardiomyocytes in vitro and non‐specific inhibition of ET‐receptors with Tezosentan caused arrhythmia and bradycardia in isolated embryonic cardiomyocytes and in whole embryonic hearts both in vitro (E10.5) and in utero (E12.5). ET‐1 mediated stimulation of early heart rate was found to occur via ETb – receptors and subsequent inositol trisphosphate receptor activation and increased SR Ca2+ leak. Conclusion ET‐1 is required to maintain a sufficient heart rate, as well as to prevent arrhythmia during early development of the mouse heart. This is achieved through ETb‐receptor, which stimulates Ca2+ leak through IP3‐receptors. This article is protected by copyright. All rights reserved.