Bovine adrenal glomerulosa (AZG) cells were shown to express bTREK-1 background K⁺ channels that set the resting membrane potential and couple Angiotensin II (AngII) receptor activation to membrane depolarization and aldosterone secretion. Northern blot and in situ hybridization studies demonstrated that bTREK-1 mRNA is uniformly distributed in the bovine adrenal cortex, including zona fasciculata and zona glomerulosa, but is absent from the medulla. TASK-3 mRNA which codes for the predominant background K⁺ channel in rat AZG cells is undetectable in the bovine adrenal cortex. In whole cell voltage clamp recordings, bovine AZG cells express a rapidly inactivating voltage-gated K⁺ current and a non-inactivating background K⁺ current with properties that collectively identify it as bTREK-1. The outwardly rectifying K⁺ current was activated by intracellular acidification, ATP, and by superfusion of bTREK-1 openers including arachidonic acid (AA) and cinnamyl 1-3,4-dihydroxy--cyanocinnamate (CDC). Bovine chromaffin cells did not express this current. In voltage and current clamp recordings, AngII (10 nM) selectively inhibited the noninactivating K⁺ current by 82.1 ± 6.1% and depolarized AZG cells by 31.6 ± 2.3 mV. CDC and AA overwhelmed AngII-mediated inhibition of bTREK-1 and restored the resting membrane potential to its control value even in the continued presence of AngII. Vasopressin (50 nM) which also physiologically stimulates aldosterone secretion inhibited the background K⁺ current by 73.8 ± 9.4 %. In contrast to its potent inhibition of bTREK-1, AngII failed to alter the T-type Ca²⁺ current (I_T-Ca) measured over a wide range of test potentials using pipette solutions of identical nucleotide and Ca²⁺-buffering compositions. AngII also failed to alter the voltage-dependence of T channel activation under these same conditions. Overall, these results identify bTREK-1 K⁺ channels as a pivotal control point where AngII receptor activation is transduced to depolarization-dependent Ca²⁺ entry and aldosterone secretion.