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International Journal of Physiology and Pathophysiology

Publicado 4 números por año

ISSN Imprimir: 2155-014X

ISSN En Línea: 2155-0158

SJR: 0.116

Physical Exercise Training Restores Constitutive NOS Coupling and Cardiac Hemodynamics in Hypertension

Volumen 7, Edición 3, 2016, pp. 199-211
DOI: 10.1615/IntJPhysPathophys.v7.i3.20
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SINOPSIS

In the heart and heart mitochondria of spontaneously hypertensive rats, we investigated the effect of physical exercise training (swimming in a moderate and excessive training mode) on the physiological indicators of cardiac hemodynamics and biochemical parameters that characterize the level of oxidative and nitrosative stress. Based on the latter, the coupling index for Ca2+-dependent constitutive NO-synthases (cNOS = eNOS + nNOS) and biochemical index of dysfunction were calculated. It turned out that in both modes of training, coupled cNOS state and Ca2+-dependent synthesis of nitric oxide (NO) were completely restored and even exceeded the reference values in untrained Wistar rats. It has been revealed that intensive regime of exercise at the breaking point of functional capability is ineffective for improving the functional state of the cardiovascular system in hypertension. Moreover, it can provoke further development of the latter. On the contrary, moderate physical training regime improves the diastolic function of the heart due to an increase in dP/dtmin, reduction of end-diastolic pressure and a significant reduction in end-diastolic stiffness. Moderate exercise decreases peripheral resistance and cardiac afterload, as indicated by the decrease in end-systolic pressure and arterial stiffness, which contribute to more efficient and energy-saving heart work, as evidenced from a decrease in stroke work at increased stroke volume. An improvement of the physiological indicators of cardiac hemodynamics and functional state of the heart in moderate mode of training correlates with changes in both calculated indices. Regular exercise training of moderate intensity is recommended as a simple physiological preconditioning method to prevent cardiac dysfunction, hypertension induced by cNOS uncoupling and excessive generation of superoxide anion and, conversely, an inhibition of Ca2+-dependent NO synthesis.

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