While cell shortening in patch clamped cells (current clamp mode) is triggered by an ordinary action potential, the trigger mechanism in field stimulated cells is not so obvious. The contraction characteristics of the two methods differ and we therefore examined the triggering sequence in field stimulated cell. Isolated rat cardiomyocytes were plated on laminin-coated cover slips which were mounted on an inverted light microscope and superfused with Hepes-Tyrodes buffer (pH 7.4; 37°C). The cells were stimulated to contract either by a 0.5 ms current injection (CC-cells) through high resistance electrodes or a 5 ms biphasic field stimulation pulse (FS-cells), and drugs were added to block sarcolemmal proteins involved in excitation-contraction coupling. Time to peak contraction (TTP) was significantly longer in FS-cells and was not affected by the polarity or the length of the stimulus pulse. Tetrodotoxin (TTX, 20µM) blocked cell shortening in CC-cells, but not in FS-cells. Ni²⁺ (5mM) blocked cell shortening in FS-cells, while KB-R7943 (KB, 5µM) had no effect either on cell shortening or TTP. In FS-cells nifedipine (Nif; 100µM) and Cd²⁺ (300µM) reduced fractional shortening by 34 and 63%, respectively, but only Cd²⁺ affected TTP (reduced by 48%). A combination of Nif and KB reduced cell shortening by 50%, while a combination of Cd²⁺ and KB almost abolished cell shortening. We conclude that field stimulation per se prolongs TTP and that cell shortening in FS-cells is not dependent on Na⁺-current (I_Na), but is triggered by a combination of L-type Ca²⁺ current and reverse mode Na⁺/Ca²⁺ exchange.