Ca 2 + -sensitising agents offer a new approach to the treatment of congestive heart failure. This study examined the effects of the Ca 2 + -sensitising agent, levosimendan, on contraction and [Ca 2 + ] i in guinea-pig ventricular myocytes. Levosimendan 100 nM produced an increase in cell shortening without affecting the [Ca 2 + ] i transient or the Ca 2 + content of the sarcoplasmic reticulum. 1 μM levosimendan increased the rate of decay of the [Ca 2 + ] i transient and increased the Ca 2 + content of the sarcoplasmic reticulum. These results suggest that at therapeutically relevant concentrations levosimendan can produce a significant inotropic effect without affecting [Ca 2 + ] i but at higher concentrations may also inhibit phosphodiesterase.