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

Tibor Rohacs, A. Spät

Research output: Contribution to journalArticle

Abstract

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 languageEnglish (US)
JournalFASEB Journal
Volume11
Issue number3
StatePublished - Dec 1 1997
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

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