The effects of Cd²⁺ (20 µM) and different bath temperatures were used to study the contributions of two separate triggering mechanisms, L-type Ca²⁺ current (I_Ca) and reverse mode Na⁺/Ca²⁺ exchange, to excitation-contraction (E-C) coupling in cat ventricular myocytes. Ionic currents and cell shortening were studied with patch pipettes filled with K⁺-containing internal solution and discontinuous ("switch") voltage clamp. Superfusion with Cd²⁺ blocked cell shortening that closely mirrored the block of I_Ca; the voltage dependence of Cd²⁺-induced reduction in contraction was bell-shaped, displaying minima at test potentials below 10 mV and above +50 mV and a maximum at about +20 mV. Cd²⁺-insensitive cell shortening was blocked by ryanodine (10 µM) and Ni²⁺ (4-5 mM). When an action potential was used as the command waveform for the voltage clamp (action potential clamp), Cd²⁺ reduced contraction to ~60 ± 7% of control cell shortening (n = 7). The remaining contraction was blocked by ryanodine and Ni²⁺. Superfusion with nifedipine (10 µM) caused nearly identical effects to Cd²⁺. The voltage dependence of contraction was sigmoidal at temperatures above 34°C but bell-shaped below 30°C. When Cd²⁺ was added to superfusate, contraction was abolished at 25°C (to 6 ± 3% of control) but reduced only modestly at 34°C (to 65 ± 13% of control, test potential +10 mV, n = 4, P < 0.01). These results indicate that 1) there is a component of contraction that is sensitive to I_Ca antagonists, and the block is equivalent with either organic or inorganic antagonists; 2) the contribution of Na⁺/Ca²⁺ exchange to triggering of contraction under our experimental conditions is fairly linear throughout the entire voltage range tested; 3) the contribution of I_Ca is superimposed on this background component contributed by the Na⁺/Ca²⁺ exchanger; and 4) triggering via the exchanger is temperature-dependent, providing a major contribution at physiological temperatures but failing at temperatures below 30°C in a nearly all-or-none fashion.