Natriuretic peptides in the pathophysiology of congestive heart failure

Research output: Contribution to journalArticle

97 Citations (Scopus)

Abstract

A hallmark of congestive heart failure (CHF) is the activation of the cardiac endocrine system, in particular atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). The natriuretic peptides are a group of structurally similar but genetically distinct peptides that have diverse actions in cardiovascular, renal, and endocrine homeostasis. ANP and BNP are of myocardial cell origin and C-type natriuretic peptide (CNP) is of endothelial origin. ANP and BNP bind to the natriuretic peptide-A receptor (NPR-A), which, via 3',5'-cyclic guanosine monophosphate (cGMP), mediates natriuresis, vasodilatation, renin inhibition, antimitogenesis, and lusitropic properties. CNP lacks natriuretic actions but possesses vasodilating and growth inhibiting actions via the guanylyl cyclase-linked natriuretic peptide-B receptor. All three peptides are cleared by the natriuretic peptide-C receptor and degraded by the ectoenzyme neutral endopeptidase 24.11, both of which are widely expressed in kidney, lung, and vascular wall. Recently, a fourth member of the natriuretic peptide, Dendroaspis natriuretic peptide (DNP) has been reported to be present in human plasma and atrial myocardium and is elevated in plasma of human CHF.

Original languageEnglish (US)
Pages (from-to)198-205
Number of pages8
JournalCurrent Cardiology Reports
Volume2
Issue number3
DOIs
StatePublished - 2000

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Natriuretic Peptides
Brain Natriuretic Peptide
Atrial Natriuretic Factor
C-Type Natriuretic Peptide
Heart Failure
Kidney
Neprilysin
Natriuresis
Peptides
Endocrine System
Peptide Receptors
Guanylate Cyclase
Cyclic GMP
Renin
Vasodilation
Blood Vessels
Myocardium
Homeostasis
Lung
Growth

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Natriuretic peptides in the pathophysiology of congestive heart failure. / Chen, Horng Haur; Burnett, John C Jr.

In: Current Cardiology Reports, Vol. 2, No. 3, 2000, p. 198-205.

Research output: Contribution to journalArticle

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