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(Hypertension. 2008;51:1273.)
© 2008 American Heart Association, Inc.

Editorial Commentaries

Aminopeptidase A

Could It Be a Novel Target for Neurogenic Hypertension?

Anderson J. Ferreira; Mohan K. Raizada

From the Department of Physiology and Functional Genomics (A.J.F., M.K.R.), College of Medicine, University of Florida, Gainesville; and the Department of Morphology (A.J.F.), Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, Brazil.

Correspondence to Mohan K Raizada, Department of Physiology and Functional Genomics, College of Medicine, University of Florida, PO Box 100274, Gainesville, FL 32610. E-mail mraizada@phys.med.ufl.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Several decades of investigation have provided unequivocal support for the existence of an intrinsic brain renin-angiotensin (Ang) system (RAS) and its involvement in the control of cardiovascular functions.^1,2 Essential components of the RAS, ie, renin, angiotensinogen, Ang-converting enzyme, Ang-converting enzyme 2, type 1 Ang II, and type 2 Ang II receptors, as well as various aminopeptidases, are synthesized within the brain, and the hyperactivity of RAS in the brain is implicated in the development and maintenance of hypertension.^1,2 Moreover, interruption of the brain RAS activity by either pharmacological or genetic means is associated with a profound beneficial outcome in hypertension.^1,2 Thus, the brain RAS may be an important target for hypertension with neurogenic origin.

Many years ago it was proposed that the physiologically relevant peptide in the brain RAS that regulates blood pressure (BP) is Ang III rather than Ang II.^3,4 Ang III, also called Ang-(2-8), is generated from Ang II by aminopeptidase A (APA), which cleaves the Asp¹-Arg² bond in Ang II. Persuasive evidence have been presented in support of this "Ang III hypothesis": (1) Ang III, when centrally administrated, enhances BP; stimulates vasopressin release, thirst, and sodium appetite; and decreases baroreceptor reflex function^3,5,6; (2) Ang III displays comparable affinity to Ang II for the type 1 Ang II receptor³; (3) specific inhibitors of APA that block the conversion of Ang III from Ang II attenuate central Ang II actions⁴ (eg, central treatment with EC33, an APA inhibitor, attenuates ICV-administrated Ang II effects on BP; in . . . [Full Text of this Article]

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