The Endocrine Function of the Heart: Physiology and Involvements of Natriuretic Peptides and Cyclic Nucleotide Phosphodiesterases in Heart Failure.

ANP BNP biomarkers clinical management cyclic nucleotide phosphodiesterase heart failure natriuretic peptides

Journal

Journal of clinical medicine
ISSN: 2077-0383
Titre abrégé: J Clin Med
Pays: Switzerland
ID NLM: 101606588

Informations de publication

Date de publication:
21 Oct 2019
Historique:
received: 23 08 2019
revised: 09 10 2019
accepted: 17 10 2019
entrez: 24 10 2019
pubmed: 24 10 2019
medline: 24 10 2019
Statut: epublish

Résumé

Besides pumping, the heart participates in hydro-sodium homeostasis and systemic blood pressure regulation through its endocrine function mainly represented by the large family of natriuretic peptides (NPs), including essentially atrial natriuretic (ANP) and brain natriuretic peptides (BNP). Under normal conditions, these peptides are synthesized in response to atrial cardiomyocyte stretch, increase natriuresis, diuresis, and vascular permeability through binding of the second intracellular messenger's guanosine 3',5'-cyclic monophosphate (cGMP) to specific receptors. During heart failure (HF), the beneficial effects of the enhanced cardiac hormones secretion are reduced, in connection with renal resistance to NP. In addition, there is a BNP paradox characterized by a physiological inefficiency of the BNP forms assayed by current methods. In this context, it appears interesting to improve the efficiency of the cardiac natriuretic system by inhibiting cyclic nucleotide phosphodiesterases, responsible for the degradation of cGMP. Recent data support such a therapeutic approach which can improve the quality of life and the prognosis of patients with HF.

Identifiants

pubmed: 31640161
pii: jcm8101746
doi: 10.3390/jcm8101746
pmc: PMC6832599
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

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Auteurs

Claire Lugnier (C)

Institute of Physiology, FMTS-EA 3072, Faculty of Medicine, University of Strasbourg, 11 Humann Street, 67000 Strasbourg, France. claire.lugnier@unistra.fr.

Alain Meyer (A)

Institute of Physiology, FMTS-EA 3072, Faculty of Medicine, University of Strasbourg, 11 Humann Street, 67000 Strasbourg, France. alain.meyer1@chru-strasbourg.fr.
Department of Physiology and Functional Explorations, New Civil Hospital, University Hospitals of Strasbourg, 1 Place de l'Hôpital, CEDEX 67091 Strasbourg, France. alain.meyer1@chru-strasbourg.fr.

Anne Charloux (A)

Institute of Physiology, FMTS-EA 3072, Faculty of Medicine, University of Strasbourg, 11 Humann Street, 67000 Strasbourg, France. anne.charloux@chru-strasbourg.fr.
Department of Physiology and Functional Explorations, New Civil Hospital, University Hospitals of Strasbourg, 1 Place de l'Hôpital, CEDEX 67091 Strasbourg, France. anne.charloux@chru-strasbourg.fr.

Emmanuel Andrès (E)

Institute of Physiology, FMTS-EA 3072, Faculty of Medicine, University of Strasbourg, 11 Humann Street, 67000 Strasbourg, France. emmanuel.andres@chru-strasbourg.fr.
Department of Internal Medicine and Metabolic Diseases, Medical Clinic B, Civil Hospital, University Hospitals of Strasbourg, 1 Place de l'Hôpital, CEDEX 67091 Strasbourg, France. emmanuel.andres@chru-strasbourg.fr.

Bernard Gény (B)

Institute of Physiology, FMTS-EA 3072, Faculty of Medicine, University of Strasbourg, 11 Humann Street, 67000 Strasbourg, France. bernard.geny@chru-strasbourg.fr.
Department of Physiology and Functional Explorations, New Civil Hospital, University Hospitals of Strasbourg, 1 Place de l'Hôpital, CEDEX 67091 Strasbourg, France. bernard.geny@chru-strasbourg.fr.

Samy Talha (S)

Institute of Physiology, FMTS-EA 3072, Faculty of Medicine, University of Strasbourg, 11 Humann Street, 67000 Strasbourg, France. samy.talha@chru-strasbourg.fr.
Department of Physiology and Functional Explorations, New Civil Hospital, University Hospitals of Strasbourg, 1 Place de l'Hôpital, CEDEX 67091 Strasbourg, France. samy.talha@chru-strasbourg.fr.

Classifications MeSH