title: [PHYSICAL EXERCISE TRAINING CAN- CELS CONSTITUTIVE NOS UNCOUPLING AND INDUCED VIOLATIONS OF CARDIAC HEMODYNAMICS IN HYPERTENSION (PART III)].
abstract: In the heart and heart mitochondria spontaneously hypertensive rats 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. The index of coupling Ca(2+)-dependent constitutive NO-synthases (cNOS = eNOS + nNOS) and biochemical index of dysfunction were calculated. It turned out that both modes of training is completely restored, and even exceed the reference values in untrained rats Wistar conjugate cNOS state and Ca(2+)-dependent synthesis of nitric oxide (NO). Intensity regime of exercise on the border of functionality have been ineffective for improving the functional state of the cardiovascular system and hypertension can provoke it further. Moderate physical training regime, on the contrary, improves the diastolic function of the heart due to an increase dP/dtmin, reducing end-diastolic pressure and a significant reduction in end-diastolic stiffness. Moderate exercise decreased peripheral resistance and cardiac afterload, as indicated by the decrease in end-systolic pressure and arterial stiffness, which contributed to more efficient and energy-saving of heart work. Improve physiological indicators of cardiac hemodynamics and functional state of the heart in moderate mode of training correlated with changes in both the calculated indices. Moderate mode of training is recommended as a simple physiological preconditioning method for the prevention of cardiac dysfunction, hypertension as a result of state uncoupling cNOS and the resulting excessive generation of superoxide and, conversely, inhibition of Ca(2+)-dependent synthesis of NO.
authors.forename: N A
authors.initials: NA
authors.lastname: Dorofeyeva
authors.forename: A V
authors.initials: AV
authors.lastname: Kotsuruba
authors.forename: B S
authors.initials: BS
authors.lastname: Kopjak
authors.forename: V F
authors.initials: VF
authors.lastname: Sagach
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000378:metabolism; D018450:Disease Progression; D017665:Hydroxyl Radical / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism* / Q000473:pathology; D017997:Leukotriene C4 / Q000378:metabolism; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D005082:Physical Exertion; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume; D013929:Thromboxane B2 / Q000378:metabolism; D014527:Uric Acid / Q000378:metabolism; D059289:Vascular Stiffness
chemical_list: D014527:Uric Acid; D017997:Leukotriene C4; D009569:Nitric Oxide; D017665:Hydroxyl Radical; D013929:Thromboxane B2; D052248:Nitric Oxide Synthase Type I; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D002118:Calcium