Initial 45Ca uptake was measured in isolated rat glomerulosa cells. A small reduction in membrane potential produced by increasing the K+ concentration from 2 to 3.6 mmol/l stimulated 45Ca uptake by about 35%, while a bigger depolarization induced by 18.5 mmol K+/l increased the uptake by about 100%. Since Ca2+ influx was already activated at a calculated membrane potential below -70 mV, and was found to be sensitive to the dihydropyridine antagonist nifedipine (1 mumol/l), but insensitive to nickel ions (100 mumol/l), it does not meet the criteria established for T- or L-type voltage-dependent Ca2+ channels. Exposure of glomerulosa cells to angiotensin II (AII) for 10 min also enhanced the rate of 45Ca influx. The effect of AII was not sensitive to 1 mumol nifedipine/l, but was strongly inhibited by 5-(N-4-chlorobenzyl)-N-(2',4'-dimethyl)benzamil (CBDMB, 30 mumol/l), an inhibitor of the Na+/Ca2+ antiporter. These observations suggest that during the sustained phase of stimulation with AII, a CBDMB-sensitive mechanism, rather than dihydropyridine-sensitive calcium channels, is involved in Ca2+ uptake in rat glomerulosa cells. The bulk Ca2+ influx did not correlate with aldosterone production; however, the maintained activity of different Ca2+ entry mechanisms seems to be essential for AII-induced aldosterone production.