1 , P.M. Coelho0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0 2 , J.P. Cordeiro0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0 1 , A.L.E.M. Assis0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0 3 , B.V. Nogueira0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0 3 , V.B. Marques0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0 4 , L. dos Santos 0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0 4 , A.P. Lima-Leopoldo 0 0 0 0 -0 0 0 0 -0 0 0 0 -0 0 0 0 1,2 AbstractNitric oxide (NO) inhibition by high-dose NG-nitro-L-arginine methyl ester (L-NAME) is associated with several detrimental effects on the cardiovascular system. However, low-dose L-NAME increases NO synthesis, which in turn induces physiological cardiovascular benefits, probably by activating a protective negative feedback mechanism. Aerobic exercise, likewise, improves several cardiovascular functions in healthy hearts, but its effects are not known when chronically associated with low-dose L-NAME. Thus, we tested whether the association between low-dose L-NAME administration and chronic aerobic exercise promotes beneficial effects to the cardiovascular system, evaluating the cardiac remodeling process. Male Wistar rats were randomly assigned to control (C), L-NAME (L), chronic aerobic exercise (Ex), and chronic aerobic exercise associated to L-NAME (ExL). Aerobic training was performed with progressive intensity for 12 weeks; L-NAME (1.5 mg Á kg -1 Á day -1 ) was administered by orogastric gavage. Low-dose L-NAME alone did not change systolic blood pressure (SBP), but ExL significantly increased SBP at week 8 with normalization after 12 weeks. Furthermore, ExL promoted the elevation of left ventricle (LV) end-diastolic pressure without the presence of cardiac hypertrophy and fibrosis. Time to 50% shortening and relaxation were reduced in ExL, suggesting a cardiomyocyte contractile improvement. In addition, the time to 50% Ca 2+ peak was increased without alterations in Ca 2+ amplitude and time to 50% Ca 2+ decay. In conclusion, the association of chronic aerobic exercise and low-dose L-NAME prevented cardiac pathological remodeling and induced cardiomyocyte contractile function improvement; however, it did not alter myocyte affinity and sensitivity to intracellular Ca 2+ handling.
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