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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 All 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 t 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 (t 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 (t 28·4±1·1 and 12·0±0·7 min). AII again increased the rate of efflux from the slow component (t = 24·2±1·7 min, P < 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 µmol/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 µmol 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.

Journal of Endocrinology (1991) 128, 297–304