Among other characteristics, the steady-state current-voltage relationship of patch-clamped single atrial myocytes from guinea-pig hearts is defined by an outward current hump in the potential region -15 to +40mV. This hump was reversibly suppressed by Co 2 + (3 mM) or nitrendipine (5 gM) and enhanced by Bay K 8644 (5 gM). The maintained outward current component suppressed by Co 2+ extended between -15.2+ 1.9mV and +39.5 _+ 1.7 mV (mean + SEM of 14 cells) and has an amplitude of 95.7 _+ 9.4 pA at + 10 inV. In isochronal I-V curves, the hump was already visible at 400 ms with essentially the same amplitude as at 1500 ms. The Co 2 +-sensitive outward current underlying the hump was poorly time-dependent during 1.5 s voltage pulses but slowly relaxed upon repolarization. Tail currents reversed near the K + equilibrium potential under our experimental conditions. The current hump of the steady-state I-V curve was also abolished by caffeine (10 raM) or ryanodine (3 gM), both drugs that interfere with sarcoplasmic reticulum function. Apamin (1 gM) or quinine (I00 gM) but not TEA (5-50 raM) markedly reduced its amplitude. However, at similar concentrations as required to inhibit the hump, both apamin and quinine appeared to be poorly specific for Ca2+-activated K + currents in heart cells since they also inhibited the L-Type Ca 2 + current. It is concluded that a long lasting CaZ+-activated outward current, probably mainly carried by K + ions but not sensitive to TEA, exists in atrial myocytes which is responsible for the current hump of the background I-V curve.