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(Circulation. 2005;112:3544-3546.)
© 2005 American Heart Association, Inc.

Editorial

Urocortin

Advancing the Neurohumoral Hypothesis of Heart Failure

John C. Burnett, Jr, MD

From the Cardiorenal Research Laboratory, Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, Minn.

Correspondence to John C. Burnett, Jr, MD, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail burnett.john@mayo.edu

Key Words: Editorials • heart failure • peptides

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

It has now been two and a half decades since the seminal study by Vaughn and coworkers demonstrating the existence of the 41–amino acid corticotropin-releasing factor (CRF), which plays a critical role in mediating the biological responses to stress.¹ In 2001, using sequence homology searching tools, Reyes et al² identified a mouse gene encoding a 38–amino acid peptide that represented a new member of the CRF peptide family, which was termed urocortin II. The biological importance in cardiovascular regulation of urocortin II was significantly advanced in 2004 by the work of Bale and colleagues,³ who reported that a genetically altered mouse model deficient of the receptor to which urocortin II binds was characterized by hypertension, whereas infusion of urocortin II into cardiomyopathic mice enhanced myocardial performance and decreased systemic vascular resistance. These works and those of others have provided increased momentum into basic and clinical research into this humoral system as it relates to cardiovascular disease, especially heart failure (HF).

Article p 3624

To date, studies have established that the CRF family consists of 3 peptides (urocortins I, II, and III), which are the binding proteins for 2 G-coupled receptors, CRF-1 and -2. Although both receptors have been localized to the central nervous system, CRF-2 is most abundant outside of the brain, particularly in the heart and vasculature. Urocortin I binds to both CRF-1 and -2, whereas urocortin II and III are the ligands for CRF-2. In addition to the work of Bale et al, reports of urocortin-like immunoreactivity in . . . [Full Text of this Article]

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