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.
|Original language||English (US)|
|State||Published - Dec 1 1997|
All Science Journal Classification (ASJC) codes
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology