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. 2015 Sep 5:412:196-204.
doi: 10.1016/j.mce.2015.05.002. Epub 2015 May 6.

Calcium-dependent mitochondrial cAMP production enhances aldosterone secretion

Dávid Katona  1 , Anikó Rajki  2 , Giulietta Di Benedetto  3 , Tullio Pozzan  3 , András Spät  4
Affiliations

Calcium-dependent mitochondrial cAMP production enhances aldosterone secretion

Dávid Katona et al. Mol Cell Endocrinol. .

Abstract

Glomerulosa cells secrete aldosterone in response to agonists coupled to Ca(2+) increases such as angiotensin II and corticotrophin, coupled to a cAMP dependent pathway. A recently recognized interaction between Ca(2+) and cAMP is the Ca(2+)-induced cAMP formation in the mitochondrial matrix. Here we describe that soluble adenylyl cyclase (sAC) is expressed in H295R adrenocortical cells. Mitochondrial cAMP formation, monitored with a mitochondria-targeted fluorescent sensor (4mtH30), is enhanced by HCO3(-) and the Ca(2+) mobilizing agonist angiotensin II. The effect of angiotensin II is inhibited by 2-OHE, an inhibitor of sAC, and by RNA interference of sAC, but enhanced by an inhibitor of phosphodiesterase PDE2A. Heterologous expression of the Ca(2+) binding protein S100G within the mitochondrial matrix attenuates angiotensin II-induced mitochondrial cAMP formation. Inhibition and knockdown of sAC significantly reduce angiotensin II-induced aldosterone production. These data provide the first evidence for a cell-specific functional role of mitochondrial cAMP.

Keywords: Aldosterone; Angiotensin II; Ca2 + signal, glomerulosa cell; Cyclic AMP; Mitochondria; Soluble adenylyl cyclase.

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