Cross-talk between aldosterone and angiotensin signaling in vascular smooth muscle cells

► Aldosterone and angiotensin II signaling pathways crosstalk in vascular smooth muscle cells. ► Some genomic effects of angiotensin II are dependent on mineralocorticoid receptor transactivation. ► Some non-genomic effects of aldosterone are dependent on angiotensin type 1 receptor (AT 1R) transact...

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Bibliographic Details
Published in:Steroids 2011-08, Vol.76 (9), p.834-839
Main Authors: Rautureau, Yohann, Paradis, Pierre, Schiffrin, Ernesto L.
Format: Article
Language:English
Subjects:
Aldosterone - metabolism
Aldosterone - physiology
Angiotensins - metabolism
Angiotensins - physiology
Animals
AT 1 receptor
Biological and medical sciences
Fundamental and applied biological sciences. Psychology
Gene Expression
Humans
Intracellular signaling
Mineralocorticoid receptor
Muscle, Smooth, Vascular - cytology
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - physiology
Myocytes, Smooth Muscle - metabolism
Myocytes, Smooth Muscle - physiology
Receptors, Angiotensin - metabolism
Receptors, Angiotensin - physiology
Receptors, Mineralocorticoid - metabolism
Receptors, Mineralocorticoid - physiology
Signal Transduction
Transcriptional Activation
Vertebrates: endocrinology
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Summary:► Aldosterone and angiotensin II signaling pathways crosstalk in vascular smooth muscle cells. ► Some genomic effects of angiotensin II are dependent on mineralocorticoid receptor transactivation. ► Some non-genomic effects of aldosterone are dependent on angiotensin type 1 receptor (AT 1R) transactivation. ► Signaling crosstalk between angiotensin II and aldosterone-stimulated pathways contributes to the vascular pathophysiological effects of the renin-angiotensin-aldosterone system. In hypertension or other forms of cardiovascular disease, the chronic activation of the renin-angiotensin-aldosterone system (RAAS) leads to dysfunction of the vasculature, including, increased vascular tone, inflammation, fibrosis and thrombosis. Cross-talk between the main mediators of the RAAS, aldosterone and angiotensin (Ang) II, participates in the development of this vascular dysfunction. Recent studies have highlighted the molecular mechanisms supporting this cross-talk in vascular smooth muscle cells (VSMCs). Some of the signaling pathways activated by the Ang II type 1 receptor (AT 1R) are dependent on the mineralocorticoid receptor (MR) and vice versa. VSMC signaling pathways involved in migration and growth are under the control of cross-talk between aldosterone and Ang II. A synergistic mechanism leads to potentiation of signaling pathways activated by each agent. The genomic and non-genomic mechanisms activated by aldosterone cooperate with Ang II to regulate vascular tone and gene expression of pro-inflammatory and pro-fibrotic molecules. This cross-talk is dependent on the non-receptor tyrosine kinase c-Src, and on receptor tyrosine kinases, EGFR and PDGFR, and leads to activation of MAP kinases and growth, migration and inflammatory effects. These new findings will contribute to development of better treatments for conditions in which the RAAS is excessively activated.
ISSN:0039-128X
1878-5867
DOI:10.1016/j.steroids.2011.02.015