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Aldosterone secretion: effect of phorbol ester and A23187
Biochemical and Biophysical Research Communications
|October 31, 1983
Summary
Angiotensin II (AII) and combined A23187/TPA treatments stimulate aldosterone secretion. The study reveals two calcium messenger system branches controlling initial and sustained secretory responses in adrenal cells.
Area of Science:
- Endocrinology
- Cell Signaling
- Molecular Biology
Background:
- Aldosterone secretion is regulated by complex signaling pathways.
- The roles of calcium and protein kinase C in this process are not fully elucidated.
Purpose of the Study:
- To compare the effects of A23187, TPA, and Angiotensin II (AII) on aldosterone secretion.
- To investigate the interplay between calcium and diacylglycerol in regulating adrenal glomerulosa cell function.
Main Methods:
- Stimulation of adrenal glomerulosa cells with AII, A23187, and TPA (12-O-tetradecanoyl-phorbol-13-acetate).
- Measurement of aldosterone secretion rates.
- Analysis of the dependence of TPA effects on intracellular free Ca2+ concentration.
Main Results:
- AII induced a prompt and sustained increase in aldosterone secretion.
- A23187 caused an initial rise followed by a decline, while TPA induced a slow, progressive increase.
- Combined A23187 and TPA treatment mimicked the sustained AII effect.
- TPA's effect was contingent on intracellular Ca2+ levels.
Conclusions:
- Two distinct branches of the calcium messenger system control aldosterone secretion.
- The calmodulin branch mediates the initial response via Ca2+ amplitude modulation.
- The C-kinase branch mediates the sustained response via diacylglycerol-induced sensitivity modulation.