Using the patch-clamp technique, we have characterised the inward current from enzymatically dispersed rabbit pulmonary arterial cells, and investigated the effects of the vasodilator, nitroprusside (NP), on these and other membrane currents. With Cs+-filled pipettes, inward currents were recorded during brief depolarizing voltage steps in both physiological Ca 2+ and 10mM Ba 2+ . The threshold for current activation was positive to -40 mV and the current peaked at 0 mV for Ca 2+ and + 10 mV for Ba 2+. During the first few minutes of recording, inward currents increased or "ran-up". This could not be attributed to blockade of outward current or the inclusion of adenosine triphosphate (ATP) in the patch pipette. Experiments revealed that all the inward current was carried through a single type of voltage-activated Ca 2+ channel, namely the high-threshold, dihydropyridine-sensitive channel. It was unaffected by tetrodotoxin but was abolished at all potentials by low concentrations of Cd 2+ (100 jIM) or nifedipine (1-2 ~M). NP (1 ~M) suppressed peak inward Ba 2+ current at + 10 mV by approximately 4507o. Higher concentrations (50 ~M) did not produce further blockade of the current. This decrease was associated with increased inactivation of the current, and both effects required the presence of ATP in the patch pipette. In physiological Ca 2+, using K+-filled pipettes, NP was found to induce spontaneous bursts of outward currents, which are probably activated by the release of Ca 2+ from Ca2+-overloaded stores. These results are consistent with NP lowering cytosolic Ca 2+, and hence causing vasodilation, by inhibiting Ca 2+ influx through voltage-gated Ca 2+ channels and by promoting Ca 2+ uptake into the sarcoplasmic reticulum.