Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 310, Issue 2, Pages H137-H152Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00618.2015
Keywords
ACE; angiotensin; heart; renin
Funding
- National Institute of Health [HL-56973, HL-51952, HD-084227, HD-047584, HD-017644]
- American Heart Association [AHA-151521, AHA-355741]
- Farley-Hudson Foundation (Jacksonville, NC)
- Groskert Heart Fund
- Wake Forest Venture Fund
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The renin-angiotensin system (RAS) constitutes a key hormonal system in the physiological regulation of blood pressure through peripheral and central mechanisms. Indeed, dysregulation of the RAS is considered a major factor in the development of cardiovascular pathologies, and pharmacological blockade of this system by the inhibition of angiotensin-converting enzyme (ACE) or antagonism of the angiotensin type 1 receptor (AT(1)R) offers an effective therapeutic regimen. The RAS is now defined as a system composed of different angiotensin peptides with diverse biological actions mediated by distinct receptor subtypes. The classic RAS comprises the ACE-ANG II-AT(1)R axis that promotes vasoconstriction; water intake; sodium retention; and increased oxidative stress, fibrosis, cellular growth, and inflammation. In contrast, the nonclassical RAS composed primarily of the ANG II/ANG III-AT(2)R and the ACE2-ANG-(1-7)-AT(7)R pathways generally opposes the actions of a stimulated ANG II-AT(1)R axis. In lieu of the complex and multifunctional aspects of this system, as well as increased concerns on the reproducibility among laboratories, a critical assessment is provided on the current biochemical approaches to characterize and define the various components that ultimately reflect the status of the RAS.
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