RESEARCH ARTICLE
The Role of Exercise on L-Arginine Nitric Oxide Pathway in Chronic Heart Failure
A.C. Mendes-Ribeiro*, 1, 2, G.E Mann3, L.R. de Meirelles1, M.B. Moss1, C. Matsuura1, T.M.C Brunini1
Article Information
Identifiers and Pagination:
Year: 2009Volume: 3
First Page: 55
Last Page: 65
Publisher ID: TOBIOCJ-3-55
DOI: 10.2174/1874091X00903010055
Article History:
Received Date: 2/7/2009Revision Received Date: 24/7/2009
Acceptance Date: 20/8/2009
Electronic publication date: 13/10/2009
Collection year: 2009
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Abstract
Chronic heart failure (CHF) is a pathological state with high morbidity and mortality and the full understanding of its genesis remain to be elucidated. In this syndrome, a cascade of neurohormonal and hemodynamic mechanisms, as well as inflammatory mediators, are activated to improve the impaired cardiac function. Clinical and experimental observations have shown that CHF is associated with a generalized disturbance in endothelium-dependent vasodilation, which may contribute to the progression of ventricular and vascular remodelling in this syndrome. There is also accumulating evidence that disturbances in nitric oxide (NO) availability is involved in the development of heart failure at the systemic and cardiac levels. NO is a ubiquitous signalling molecule which causes potent vasodilation, inhibits platelet activation and regulates the contractile properties of cardiac myocytes. It is generated from the amino acid L-arginine via constitutive and inducible isoforms of the enzyme NO synthase (NOS). There is evidence that exercise, a nonpharmacological tool, improves symptoms, fitness (VO2peak), quality of life and NO bioavailability in CHF population. This review examines different aspects of the L-arginine-NO pathway and inflammation in the physiopathology of CHF and highlights the important beneficial effects of exercise in this disease.
