Various cardio‐active stimuli, including endothelin‐1 (ET‐1), exhibit potent arrhythmogenicity, but the underlying cellular mechanisms of their actions are largely unclear. We used isolated rat atrial myocytes and related changes in their subcellular Ca²⁺ signalling to the ability of various stimuli to induce diastolic, premature extra Ca²⁺ transients (ECTs). For this, we recorded global and spatially resolved Ca²⁺ signals in indo‐1‐ and fluo‐4‐loaded atrial myocytes during electrical pacing. ET‐1 exhibited a higher arrhythmogenicity (arrhythmogenic index; ratio of number of ECTs over fold‐increase in Ca²⁺ response, 8.60; n= 8 cells) when compared with concentrations of cardiac glycosides (arrhythmogenic index, 4.10; n= 8 cells) or the β‐adrenergic agonist isoproterenol (arrhythmogenic index, 0.11; n= 6 cells) that gave similar increases in the global Ca²⁺ responses. Seventy‐five percent of the ET‐1‐induced arrhythmogenic Ca²⁺ transients were accompanied by premature action potentials, while for digoxin this proportion was 25 %. The β‐adrenergic agonist failed to elicit a significant number of ECTs. Direct activation of inositol 1,4,5‐trisphosphate (InsP₃) receptors with a membrane‐permeable InsP₃ ester (InsP₃ BM) mimicked the effect of ET‐1 (arrhythmogenic index, 14.70; n= 6 cells). Inhibition of InsP₃ receptors using 2 μM 2‐aminoethoxydiphenyl borate, which did not display any effects on Ca²⁺ signalling under control conditions, specifically suppressed the arrhythmogenic action of ET‐1 and InsP₃ BM. Immunocytochemistry indicated a co‐localisation of peripheral, junctional ryanodine receptors with InsP₃Rs. Thus, the pronounced arrhythmogenic potency of ET‐1 is due to the spatially specific recruitment of Ca²⁺ sparks by subsarcolemmal InsP₃Rs. Summation of such sparks efficiently generates delayed afterdepolarisations that trigger premature action potentials. We conclude that the particular spatial profile of cellular Ca²⁺ signals is a major, previously unrecognised, determinant for arrhythmogenic potency and that the InsP₃ signalling cassette might therefore be a promising new target for understanding and managing atrial arrhythmia.