We have detected two inwardly rectifying potassium conductances in AtT-20 clonal corticotrophs, a cell line derived from the mouse pituitary gland. An agonist-independent potassium conductance was activated by voltage steps negative to the reversal potential for potassium (VK) and was completely blocked by 1 mM barium in the bathing solution. The conductance was transient and inactivated completely with a time constant of about 80 ms. Reducing the external sodium concentration from 140 mM to 14 mM attenuated inactivation. In the presence of 100 nM somatostatin an inwardly rectifying conductance, which reversed at potentials close to VK, was also elicited. This conductance exhibited a maximal slope conductance that increased with increasing extracellular potassium. Rectification depends on both voltage and extracellular potassium concentration (Vm-VK). The inward current induced by somatostatin during voltage steps negative to VK was completely blocked by 1 mM extracellular barium, whereas the outward somatostatin-induced current activated at the holding current, which was about 30 mV positive to VK, was unaffected by 1 mM extracellular barium. The muscarinic agonist carbachol (10 microM) also induces an inwardly rectifying conductance of similar magnitude to that induced by somatostatin. Since the agonist-independent potassium current exhibits sodium-dependent inactivation, whereas the hormone-induced current does not inactivate, these currents are probably carried by different populations of potassium channels.