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Efflux of potassium ions in angiotensin II-stimulated bovine adrenocortical cells.

Angiotensin II (AII) stimulation of steroidogenesis is known to be associated with depolarization of the adrenocortical cell membrane. In these cells, membrane permeability to potassium ions governs electrical potential. The effects of AII on the rate of efflux of K+ in relation to the control of aldosterone synthesis has been investigated in bovine adrenocortical cells preloaded with 43K. In static incubations, the pattern of 43K efflux fitted a model with two exponential components with t1/2 values of 47.7 +/- 1.7 and 14.2 +/- 0.6 (S.E.M.) min. AII increased the efflux rate of the slow-exchange component (t1/2 37.1 +/- 0.6 min) and retarded efflux from the fast-exchange component. With ouabain present to prevent reuptake of the isotope, the rate of efflux for both components was increased in unstimulated cells (t1/2 28.4 +/- 1.1 and 12.0 +/- 0.7 min). AII again increased the rate of efflux from the slow component (t1/2 = 24.2 +/- 1.7 min, P less than 0.01) and retarded efflux from the fast component. These biphasic effects were apparent in cells treated with a range of AII concentrations (0.1 nmol/l-1 mumol/l) but the point in time at which increased efflux from the slower component predominated over retardation of the slow component was earlier for cells treated with 1 mumol AII/l than for cells treated with lower concentrations. We suggest that decreases and increases in K+ efflux caused by AII are associated with depolarization and repolarization respectively. Changes in intracellular concentrations of Ca2+ may link these events.