Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/12298
Title: From gene to protein-experimental and clinical studies of ACE2 in blood pressure control and arterial hypertension.
Authors: Patel, Sheila K;Velkoska, Elena;Freeman, Melanie;Wai, Bryan;Lancefield, Terase F;Burrell, Louise M
Affiliation: Department of Medicine, Austin Health, University of Melbourne Heidelberg, VIC, Australia.
Department of Medicine, Austin Health, University of Melbourne Heidelberg, VIC, Australia ; Department of Cardiology, Austin Health, University of Melbourne Heidelberg, VIC, Australia.
Department of Medicine, Austin Health, University of Melbourne Heidelberg, VIC, Australia ; Department of Cardiology, Austin Health, University of Melbourne Heidelberg, VIC, Australia ; Department of Cardiology, The Northern Hospital, University of Melbourne Epping, VIC, Australia.
Issue Date: 24-Jun-2014
Citation: Frontiers in Physiology 2014; 5(): 227
Abstract: Hypertension is a major risk factor for stroke, coronary events, heart and renal failure, and the renin-angiotensin system (RAS) plays a major role in its pathogenesis. Within the RAS, angiotensin converting enzyme (ACE) converts angiotensin (Ang) I into the vasoconstrictor Ang II. An "alternate" arm of the RAS now exists in which ACE2 counterbalances the effects of the classic RAS through degradation of Ang II, and generation of the vasodilator Ang 1-7. ACE2 is highly expressed in the heart, blood vessels, and kidney. The catalytically active ectodomain of ACE2 undergoes shedding, resulting in ACE2 in the circulation. The ACE2 gene maps to a quantitative trait locus on the X chromosome in three strains of genetically hypertensive rats, suggesting that ACE2 may be a candidate gene for hypertension. It is hypothesized that disruption of tissue ACE/ACE2 balance results in changes in blood pressure, with increased ACE2 expression protecting against increased blood pressure, and ACE2 deficiency contributing to hypertension. Experimental hypertension studies have measured ACE2 in either the heart or kidney and/or plasma, and have reported that deletion or inhibition of ACE2 leads to hypertension, whilst enhancing ACE2 protects against the development of hypertension, hence increasing ACE2 may be a therapeutic option for the management of high blood pressure in man. There have been relatively few studies of ACE2, either at the gene or the circulating level in patients with hypertension. Plasma ACE2 activity is low in healthy subjects, but elevated in patients with cardiovascular risk factors or cardiovascular disease. Genetic studies have investigated ACE2 gene polymorphisms with either hypertension or blood pressure, and have produced largely inconsistent findings. This review discusses the evidence regarding ACE2 in experimental hypertension models and the association between circulating ACE2 activity and ACE2 polymorphisms with blood pressure and arterial hypertension in man.
Internal ID Number: 25009501
URI: http://ahro.austin.org.au/austinjspui/handle/1/12298
DOI: 10.3389/fphys.2014.00227
URL: http://www.ncbi.nlm.nih.gov/pubmed/25009501
Type: Journal Article
Subjects: angiotensin converting enzyme
angiotensin converting enzyme 2
blood pressure
hypertension
renin angiotensin system
Appears in Collections:Journal articles

Files in This Item:
There are no files associated with this item.


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.