The perforated‐patch‐clamp technique was used to identify an inwardly rectifying K+ current (IK(IR)) in cultured rat anterior pituitary cells highly enriched in corticotropes. IK(IR) was rapidly activating and highly selective for K+. The K+ conductance was approximately proportional to the square root of the extracellular K+ concentration. I K(IR) was blocked in a voltage‐dependent manner by external Ba2+ and Cs+, slightly attenuated by 5 mM 4‐aminopyridine (15% inhibition) and insensitive to 10 mM tetra‐ethylammonium, 2 mM Ca2+, 1 mM Cd2+ and 50 μM La3+. In physiological saline, 100 μM Ba2+, which inhibits 86% of IK(IR) at the cell resting potential, depolarized cells by 6.1 ± 0.7 mV from a mean resting potential of −59.6 ± 0.8 mV. Corticotropin releasing hormone (CRH), which activates adenylyl cyclase and stimulates adrenocorticotropic hormone (ACTH) secretion from corticotropes, inhibited IK(IR) by 25% and depolarized the cells by 10.2 ± 1.0 mV. Dibutyryl cAMP ((Bu)2cAMP) mimicked these effects. The membrane depolarization evoked by Ba2+ or CRH increased the cell firing frequency. Comparison of cells exhibiting a membrane potential of approximately −50 mV revealed that spike frequency in the presence of CRH (109 ± 7 spikes (5 min)−1) was greater than in control (60 ± 5 spikes (5 min)−1) or Ba2+‐treated (77 ± 15 spikes (5 min)−1) corticotropes. The data suggest that IK(IR) contributes to maintenance of the resting membrane potential of rat corticotropes. Inhibition of IK(IR) plays a role in, but does not account for all of, the membrane depolarization and enhancement of firing frequency evoked by CRH.