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Intracellular calcium: a prerequisite for aldosterone action.
C Schäfer1, V Shahin, L Albermann
1Institute of Physiology I, Nanolab, University Münster, Robert-Koch-Str. 27a, D-48149 Münster, Germany.
The Journal of Membrane Biology
|January 16, 2004
Summary
Intracellular calcium (Ca2+) is essential for the genomic effects of the hormone aldosterone, influencing early steps in the signaling pathway. This finding highlights calcium
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Physiology
Background:
- Aldosterone regulates salt and water transport via mineralocorticoid receptors.
- Aldosterone initiates genomic responses through nuclear receptor translocation and transcription.
- Rapid, pre-genomic aldosterone effects involve increased intracellular calcium (Ca2+).
Purpose of the Study:
- To investigate the role of intracellular Ca2+ in aldosterone's genomic signaling pathway.
- To determine if Ca2+ is required for aldosterone receptor binding, nuclear translocation, or transcription.
Main Methods:
- Electrophysiological measurements of nuclear envelope electrical resistance in Xenopus laevis oocytes.
- Aldosterone exposure with and without the Ca2+ chelator EGTA.
- Assessment of transcription inhibition using actinomycin D.
Main Results:
- EGTA abolished all aldosterone-induced electrical responses across the nuclear envelope.
- Actinomycin D blocked transcription-dependent responses (transient drop and late peak) but not the early peak.
- Aldosterone-evoked nuclear envelope electrical resistance changes were dependent on intracellular Ca2+.
Conclusions:
- Intracellular Ca2+ is a prerequisite for the genomic action of aldosterone.
- Calcium ions play an early role in the aldosterone signaling cascade, potentially in receptor binding or nuclear pore complex interaction.