Authors: Paul J. Lijnen; Victor V. Petrov; Robert H. Fagard

Source: Vascular Disease Prevention, Volume 1, Number 3, November 2004 , pp. 175-184(10)

Publisher: Bentham Science Publishers

Abstract:

The heart is a major site of natriuretic peptides (NP). Atrial and brain natriuretic peptide (ANP and BNP) are predominantly produced by atria and ventricles. C-Natriuretic peptide (CNP) is also found in heart tissue. ANP and BNP are produced by cardiomyocytes and fibroblasts. Cardiac fibroblasts also secrete CNP. Three NP-receptors (NPR-A, NPRB, NPR-C) are expressed in heart atria and ventricles.

ANP, BNP and CNP exert antihypertrophic actions in cardiomyocytes, suppress cardiac fibroblast growth and inhibit collagen synthesis in cardiac fibroblasts. In vivo infusion of ANP also reduces collagen deposition in the arterial wall of spontaneously hypertensive rats.

Baseline plasma BNP is a sensitive predictor of morbidity and mortality in heart failure and changes in BNP over time are associated with corresponding changes in subsequent mortality and morbidity. Plasma BNP, and to a lesser extent ANP, is also a strong cardiovascular risk marker in patients with essential hypertension and left ventricular hypertrophy without left ventricle dysfunction or overt renal disease. A potential role for genetic variants of the ANP gene in the modulation of the disease phenotype observed with some cardiovascular diseases is also reported. Neutral endopeptidase inhibition may also have inhibitory effects on cardiac hypertrophy and fibrosis.

Keywords: natriuretic peptides; cardiac hypertrophy; myocardial fibrosis; infarction; heart failure; neutral endopeptidase inhibition

Document Type: Review article

DOI: http://dx.doi.org/10.2174/1567270043404791

Affiliations: 1: Hypertension Unit, Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.

Publication date: 2004-11-01

More about this publication?

• Vascular Disease Prevention publishes reviews as well as original papers to update all those concerned with this topic at the clinical or scientific level. In addition to clinically relevant topics, we consider reviews and original papers dealing with the more scientific aspects of vascular disease prevention. This includes the evaluation of emerging vascular risk factors, research dealing with the pathogenesis of atherosclerosis and the investigation of new treatment options both at the clinical and scientific level (e.g. epidemiology, patient-based studies, experimental models, in vitro experiments or molecular research). Therefore, another function of Vascular Disease Prevention is to bridge the gap between clinical practice and ongoing laboratory-based research.
  
  In particular, we welcome critical reviews and comments on recent trials. This is a topic that requires regular updates because of the large number of trials published every year.
  
  Debates are encouraged in the correspondence section of this journal.
  The editorial structure of Vascular Disease Prevention is set up with the aim of dealing with the submitted material as rapidly as possible. Specialist editors will provide a more expert and rapid assessment unlike a more centralized editorial structure.

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