ObjectiveThe observation of local ‘elementary’ Ca2+release events (Ca2+sparks) through ryanodine receptor (RyR) channels in the sarcoplasmic reticulum (SR) has changed our understanding of excitation–contraction (EC) coupling in cardiac and smooth muscle. In arterial smooth muscle, Ca2+sparks have been suggested to oppose myogenic vasoconstriction and to influence vasorelaxation by activating co-localized Ca2+activated K+(KCa) channels (STOCs). However, all prior studies on Ca2+sparks have been performed in non-human tissues.MethodsIn order to understand the possible significance of Ca2+sparks to human cardiovascular function, we used high spatial resolution confocal imaging to record Ca2+sparks in freshly-isolated, individual myocytes of human coronary arteries loaded with the Ca2+indicator fluo-3.ResultsLocal SR Ca2+release events recorded in human myocytes were similar to ‘Ca2+sparks’ recorded previously from non-human smooth muscle cells. In human myocytes, the peak [Ca2+]iamplitudes of Ca2+sparks (measured as F/F0) and width at half-maximal amplitude were 2.3 and 2.27 μm, respectively. The duration of Ca2+sparks was 62 ms. Ca2+sparks were completely inhibited by ryanodine (10 μmol/l). Ryanodine-sensitive STOCs could be identified with typical properties of KCachannels activated by Ca2+sparks.ConclusionOur data implies that modern concepts suggesting an essential role of Ca2+spark generation in EC coupling recently derived from non-human muscle are applicable to human cardiovascular tissue. Although the basic properties of Ca2+sparks are similar, our results demonstrate that Ca2+sparks in coronary arteries in humans, have features distinct from non-arterial smooth muscle cells of other species.