The hypothesis that Ca²⁺ influx necessary for angiotensin II (AngII) and K⁺ stimulation of aldosterone secretion is primarily mediated by membrane depolarization and activation of T-type Ca²⁺ channels was examined in isolated rat adrenal glomerulosa cells. Perforated-patch clamp recordings of membrane potential (V_m) demonstrated that AngII and K⁺ induce concentration-dependent depolarizations capable of activating T channels and, at high K⁺ and AngII concentrations, activating L channels and inactivating T channels. K⁺-induced depolarizations were stable and readily reversible. V_m was proportional to K⁺ concentration, exhibiting a linear slope of 53.7 mV per 10-fold increase in K⁺. AngII-induced depolarizations were complex, consisting of a slow maintained component superimposed with small amplitude depolarizing fluctuations. Slow oscillations in V_m were occasionally observed in response to 10⁻⁹ M AngII or greater. The slow, maintained component of depolarization coincided with inhibition of K⁺ conductance. Neither rapid fluctuations nor slow oscillations in V_m were blocked by mibefradil or other treatments that inhibit voltage-gated Ca²⁺ channels. Perforated-patch clamp experiments also demonstrated that AngII (10⁻⁸ M) inhibited L channels by 45.6% without affecting T channels. Thus AngII activates T channels by depolarization rather than T channel modulation in rat cells. The concentration dependencies of mibefradil inhibition of T channels and AngII- and K⁺-induced aldosterone secretion were compared. Under whole-cell patch clamp mibefradil induced a concentration-dependent inhibition of T channels, exhibiting a K_app of 0.62 μM. Mibefradil inhibition was use-dependent but mibefradil neither acted as an open channel blocker nor significantly affected T channel inactivation or activation. Mibefradil inhibited K⁺- and AngII-induced secretion at concentrations similar to that for T channel inhibition; at high concentrations (10 μM) mibefradil inhibited AngII-induced secretion by 88% and completely inhibited K⁺-induced secretion. The IC₅₀ for K⁺-induced secretion was dependent on K⁺ concentration, increasing from 0.2 μM for 6 mM K⁺ to 2.5 μM for 10 mM K⁺ or greater. Mibefradil exhibited an IC₅₀ of 1.1 μM for inhibition of secretion at all AngII concentrations examined (0.1, 1.0, and 10 nM). Mibefradil also exhibited multiple nonspecific effects, which complicated the assessment of T channel function, including; inhibition of leak and voltage-dependent K⁺ conductances, inhibition of Ca²⁺-independent aldosterone secretion, and inhibition of secretion under conditions expected to completely inactivate T channels (10 nM AngII or 20 mM K⁺). In summary, these results indicate that voltage-gated T channels represent the primary Ca²⁺ influx pathway activated by physiological concentrations of AngII and K⁺ but other Ca²⁺ influx pathways must mediate aldosterone secretion induced by high K⁺ or AngII concentrations.