Nongenomic effects of aldosterone

Genomic effects of aldosterone are those at the nuclear level through transcription after binding to mineralocorticoid receptors. Effects on mineralocorticoid receptors other than those on the nucleus are nongenomic. Nongenomic effects of aldosterone can also involve other receptors like the G-protein-coupled estrogen receptor (GPER), which is responsible for increase in LDL receptors, decrease in LDL cholesterol, decrease in gluconeogenesis, decrease in lipogenesis and decreased triglyceride storage. Other effects through GPER are vasodilatation due to endothelial nitric oxide, increase in apoptosis, decrease in vascular remodeling, vascular injury and cell proliferation and migration [1]. Other nongenomic effects are increases in reactive oxidative species, increased calcium levels, inflammation, elastin production and the regulation of sodium and pH. Nongenomic pathways are rapid acting through caveolin-1, striatin and activation of GPER and extracellular signal-related protein kinase 1 or 2 [2].

References

1. Fioretti F, Testani JM, Tio MC, Pitt B, Butler J. Aldosterone and Aldosterone Modulation in Cardio-Kidney Diseases. J Am Coll Cardiol. 2025 Aug 5;86(5):354-373. doi: 10.1016/j.jacc.2025.06.012. PMID: 40738563.
2. Dooley R, Harvey BJ, Thomas W. Non-genomic actions of aldosterone: from receptors and signals to membrane targets. Mol Cell Endocrinol. 2012 Mar 24;350(2):223-34. doi: 10.1016/j.mce.2011.07.019. Epub 2011 Jul 27. PMID: 21801805.