Inositol‐1,4,5‐trisphosphate (IP₃)‐dependent Ca²⁺ release represents the major Ca²⁺ mobilizing pathway responsible for diverse functions in non‐excitable cells. In the heart, however, its role is largely unknown or controversial. In intact cat atrial myocytes, endothelin (ET‐1) increased basal [Ca²⁺]_i levels, enhanced action potential‐evoked [Ca²⁺]_i transients, caused [Ca²⁺]_i transients with alternating amplitudes (Ca²⁺ alternans), and facilitated spontaneous Ca²⁺ release from the sarcoplasmic reticulum (SR) in the form of Ca²⁺ sparks and arrhythmogenic Ca²⁺ waves. These effects were prevented by the IP₃ receptor (IP₃R) blocker aminoethoxydiphenyl borate (2‐APB), suggesting the involvement of IP₃‐dependent SR Ca²⁺ release. In saponin‐permeabilized myocytes IP₃ and the more potent IP₃R agonist adenophostin increased basal [Ca²⁺]_i and the frequency of spontaneous Ca²⁺ sparks. In the presence of tetracaine to eliminate Ca²⁺ release from ryanodine receptor (RyR) SR Ca²⁺ release channels, IP₃ and adenophostin triggered unique elementary, non‐propagating IP₃R‐dependent Ca²⁺ release events with amplitudes and kinetics that were distinctly different from classical RyR‐dependent Ca²⁺ sparks. The effects of IP₃ and adenophostin were prevented by heparin and 2‐APB. The data suggest that IP₃‐dependent Ca²⁺ release increases [Ca²⁺]_i in the vicinity of RyRs and thus facilitates Ca²⁺‐induced Ca²⁺ release during excitation–contraction coupling. It is concluded that in the adult mammalian atrium IP₃‐dependent Ca²⁺ release enhances atrial Ca²⁺ signalling and exerts a positive inotropic effect. In addition, by facilitating Ca²⁺ release, IP₃ may also be an important component in the development of Ca²⁺‐mediated atrial arrhythmias.