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Critical Reviews™ in Eukaryotic Gene Expression
IF: 2.156 5-Year IF: 2.255 SJR: 0.649 SNIP: 0.599 CiteScore™: 3

ISSN Print: 1045-4403
ISSN Online: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukaryotGeneExpr.v14.i12.70
10 pages

Circulating versus Local Angiotensin II in Blood Pressure Control: Lessons from Tissue-Specific Expression of Angiotensin-Converting Enzyme (ACE)

Hong D. Xiao
Department of Pathology, Emory University, Atlanta, GA 30322
Sebastien Fuchs
Department of Pathology, Emory University, Atlanta, GA 30322
Kristen Frenzel
Department of Pathology, Emory University, Atlanta, GA 30322
Lu Teng
Department of Pathology, Emory University, Atlanta, GA 30322
Kenneth E. Bernstein
Department of Pathology, Emory University, Atlanta, GA 30322

ABSTRACT

The renin angiotensin system (RAS) is a central player in blood pressure control. Its effector peptide, angiotensin II, regulates blood pressure through coordinated actions in multiple tissues. The RAS is generally considered to be an endocrine system, and angiotensin II to be a circulating hormone. In recent years, however, a role for locally produced angiotensin II has been proposed. The major site for angiotensin II production is endothelium, where angiotensin-converting enzyme (ACE) is abundantly expressed. To elucidate the relative importance of circulating angiotensin II versus locally produced angiotensin II, one approach is to create a mouse model in which ACE is expressed in a tissue-specific manner. In this review, we discuss strategies to create such a model. In a mouse model we generated using a novel promoter-swapping technique, the endothelial ACE is eliminated and replaced by ectopic production of ACE in the liver. This model specifically addresses the question of whether local production of angiotensin II is essential for RAS function.


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