Sustained stimulation of aldosterone production by angiotensin II is potentiated by nickel

Angiotensin-induced aldosterone production by superfused adrenal glomerulosa cells was potentiated by Ni2+ (0.1 mM), added either at the onset of stimulation with angiotensin II or 1 h later. Nickel did not influence the effect of adrenocorticotropic hormone or potassium on aldosterone production. Nickel failed to modify angiotensin-induced changes in phospholipid metabolism or the formation of inositol phosphates and slightly reduced the enhancement of 45Ca influx. Uptake of Ni2+ into glomerulosa cells was increased by depolarization in a dihydropyridine-insensitive manner. Because nickel selectively potentiates the sustained phase of the response to a calcium-mobilizing hormone, it may serve as a suitable tool in elucidating the signal transduction process during the sustained phase of stimulation.