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
1 Departamento de Farmacologia e Psicobiologia, Instituto de Biologia, Av. 28 de Setembro 87 CEP 20551-030, Rio de Janeiro, Brazil
2 Disciplina de Farmacologia, Departamento de Ciências Fisiológicas, Universidade Federal do Estado do Rio de Janeiro, Rio de Janeiro, Brazil
3 Cardiovascular Division, School of Biomedical and Health Sciences, King’s College London, Guy's Campus, London, UK
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.
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