Aim Activity of early embryonic cardiomyocytes relies on spontaneous Ca2+ oscillations that are induced by interplay between sarcoplasmic reticulum (SR) – Ca2+ release and ion currents of the plasma membrane. In a variety of cell types, Ca2+‐activated K+ current (IK(Ca)) serves as a link between Ca2+ signals and membrane voltage. This study aimed to determine the role of IK(Ca) in developing cardiomyocytes. Methods Ion currents and membrane voltage of embryonic (E9‐11) mouse cardiomyocytes were measured by patch clamp; [Ca2+]i signals by confocal microscopy. Transcription of specific genes was measured with RT‐qPCR and Ca2+‐dependent transcriptional activity using NFAT‐luciferase assay. Myocyte structure was assessed with antibody labelling and confocal microscopy. Results E9‐11 cardiomyocytes express small conductance (SK) channel subunits SK2 and SK3 and have a functional apamin‐sensitive K+ current, which is also sensitive to changes in cytosolic [Ca2+]i. In spontaneously active cardiomyocytes, inhibition of IK(Ca) changed action and resting potentials, reduced SR Ca2+ load and suppressed the amplitude and the frequency of spontaneously evoked Ca2+ oscillations. Apamin caused dose‐dependent suppression of NFAT‐luciferase reporter activity, induced downregulation of a pattern of genes vital for cardiomyocyte development and triggered changes in the myocyte morphology. Conclusion The results show that apamin‐sensitive IK(Ca) is required for maintaining excitability and activity of the developing cardiomyocytes as well as having a fundamental role in promoting Ca2+‐ dependent gene expression.