Cytoplasmic Ca²⁺ and mitochondrial NAD(P)H signal in adrenal glomerulosa cells

We measured mitochondrial NAD(P)H simultaneously with cytoplasmic [Ca²⁺] ([Ca²⁺]_i) in single glomerulosa cells by microfluorimetry to asses their kinetic correlation. K⁺ induced parallel elevation of [Ca²⁺]_i and mitochondrial NAD(P)H. The NAD(P)H response reached the peak slower and decayed slower upon the removal of K⁺ than [Ca²⁺]_i, suggesting that the NAD(P)H signal is the consequence of Ca²⁺ signal. Low concentrations of AII induced parallel oscillations both in [Ca²⁺]_i and NAD(P)H. Sustained elevation of [Ca²⁺]_i evoked by either K⁺ or higher concentration of All induced a sustained NAD(P)H signal. It was probably the consequence of a sustained mitochondrial Ca²⁺ signal, as long lasting elevation of extramitochondrial [Ca²⁺] evoked a sustained rise in intramitochondrial [Ca²⁺] as measured whit rhod-2. Inhibition of aldosterone production by aminoglutethimide reduced the slope of decay of the NAD(P)H signal upon the removal of K⁺, indicating that NADPH is consumed significantly by steroid synthesis. The strong correlation of the kinetics of Ca²⁺ and NAD(P)H signal and the rapid consumption of the latter by aldosterone synthesis suggest an important role of this mechanism in steroid secretion.