Adrenal zona glomerulosa (ZG) cells produce aldosterone in response to angiotensin II and extracellular potassium through different mechanisms which involve changes in cytosolic free calcium (Cai). Protein kinase C (PKC) activation is part of the angiotensin II signalling cascade but its effects on Cai are unknown. PKC activation with 1 microM phorbol 12-myristate 13-acetate (PMA) and 8 mM Ko significantly increased the rate of calcium influx (P < 0.001). Both the PKC- and the Ko-induced calcium influx occurred via a nifedipine-sensitive pathway. When both were combined, PKC activation and 8 mM Ko were not additive over either agent alone. PKC activation and 8 mM Ko also stimulated calcium efflux (P < 0.01). When combined together PKC activation and 8 mM Ko had additive effects on calcium efflux (P < 0.05). PKC activation did not increase Cai nor the exchangeable calcium pool in contrast to 8 mM Ko which significantly increased both (P < 0.001). Thus, PKC activation in ZG cells induces a pattern of calcium transport characterized by accelerated calcium recycling across the cell membrane without increasing cell calcium content.