title: Aldosterone and the risk of hypertension.
abstract: Aldosterone, the key hormone in the mineralocorticoid pathway, plays a fundamental role in salt and water homeostasis, blood pressure regulation, and cardiovascular remodeling. Both genomic and nongenomic mechanisms influence aldosterone-induced renal sodium reabsorption. Furthermore, the mineralocorticoid receptors in nonepithelial tissues, including the heart and vascular smooth muscle cells, have recently been discovered. Thus, aldosterone likely has pleiotropic effects that contribute to the modulation of blood pressure. Among patients with hypertension in general, and among those with more severe or resistant hypertension in particular, a higher-than-expected prevalence of primary hyperaldosteronism is noted. Among individuals with resistant hypertension, aldosterone antagonists have also been shown to be effective in lowering blood pressure. Most significantly, recent community-based studies among non-hypertensive individuals in the general population have demonstrated that both higher serum aldosterone concentrations and a higher aldosterone to renin ratio portend a greater risk of developing hypertension. The combination of the aforementioned observations underscores the importance of the mineralocorticoid pathway in the pathogenesis of hypertension.
authors: Section of Preventive Medicine and Epidemiology, Boston University School of Medicine, 801 Massachusetts Avenue, Suite 470, Boston, MA 02118, USA. vanessax@bu.edu
authors: Vanessa
authors: V
authors: Xanthakis
authors: Ramachandran S
authors: RS
authors: Vasan
mesh_terms: D000450:Aldosterone / Q000502:physiology*; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications*; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D012083:Renin / Q000378:metabolism
chemical_list: D000451:Mineralocorticoid Receptor Antagonists; D000450:Aldosterone; D012083:Renin
references: Can J Cardiol. 2012 May;28(3):318-25
references: 22521297
references: J Clin Endocrinol Metab. 2000 Jun;85(6):2160-6
references: 10852446
references: Postgrad Med. 2012 Jan;124(1):67-73
references: 22314116
references: Lancet. 2001 Mar 24;357(9260):953-4
references: 11289366
references: Am J Hypertens. 2005 May;18(5 Pt 1):657-65
references: 15882548
references: J Clin Endocrinol Metab. 2008 Sep;93(9):3266-81
references: 18552288
references: Hypertension. 1996 Dec;28(6):927-36
references: 8952579
references: Cardiovasc Res. 1983 Aug;17(8):437-45
references: 6352032
references: N Engl J Med. 2004 Jul 1;351(1):33-41
references: 15229305
references: J Clin Endocrinol Metab. 2006 Feb;91(2):454-9
references: 16291704
references: J Am Coll Cardiol. 2005 Apr 19;45(8):1243-8
references: 15837256
references: Neth J Med. 2008 May;66(5):220-8
references: 18490805
references: J Vasc Res. 2013;50(2):89-99
references: 23172373
references: Hypertension. 2007 Apr;49(4):846-56
references: 17296870
references: J Hypertens. 2012 Dec;30(12):2322-30
references: 23107914
references: Eur J Cardiovasc Prev Rehabil. 2011 Aug;18(4):664-73
references: 21450637
references: J Mol Med (Berl). 2012 May;90(5):495-508
references: 22527880
references: Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14211-6
references: 14614137
references: Mol Cell Endocrinol. 2012 Mar 24;350(2):151-62
references: 21839803
references: Am J Hypertens. 2012 May;25(5):514-23
references: 22258336
references: J Clin Endocrinol Metab. 1999 Nov;84(11):4031-6
references: 10566645
references: Eur J Endocrinol. 2012 Jul;167(1):7-15
references: 22495491
references: J Hypertens. 2012 Oct;30(10):1899-902
references: 22929608