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- W2898879140 abstract "Objectives: Phosphorylation of p66shc is known to be mediated oxidative stress in many cell types and tissues. In the vasculature, p66shc plays a pivotal role in endothelial dysfunction associated with pathophysiological conditions such as hypertension. We investigated the role of endurance exercise training on p66shc phosphorylation in aorta of Spontaneously Hypertensive Rats (SHRs). Methods: Eight week old SHRs and Wistar-Kyoto rats (WKY) were randomly divided into 3 groups: Wistar-Kyoto rats (WKY, n = 10), SHR control (SHR-C, n = 10), and SHR endurance exercise training (SHR-E, n = 10). Endurance exercise training was performed on a treadmill (12–20 m/min, 0% grade, 60 min/day, 5 days/week, 16 weeks). Results: Endurance exercise training significantly improved arterial blood pressure, endothelial dependent relaxation, central pulse wave velocity (cPWV), and superoxide production in aorta of SHR compared with SHR-C. Phosphorylation of PCKbetaII and p66shc (S36) in SHR-C were significantly higher than in WKY, but it was recovered by endurance exercise training (SHR-E) compared to SHR-C (p < .05) without changes of total PCKbetaII and p66shc in aorta of SHR. Also, endothelial nitric oxide synthase (eNOS) phosphorylation and manganese superoxide dismutase (MnSOD) expression were significantly increased by endurance exercise training (SHR-E vs SHR-C, p < .05) in aorta of SHR. Conclusion: these data suggest that endurance exercise training suppresses blood pressure via reduction of PCKbetaII and p66shc phosphorylation and enhancement of eNOS and MnSOD expression in SHR." @default.
- W2898879140 created "2018-11-09" @default.
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- W2898879140 date "2018-10-01" @default.
- W2898879140 modified "2023-09-25" @default.
- W2898879140 title "A8543 Endurance Exercise training attenuates blood pressure via suppression of p66shc phosphorylation in Spontaneously hypertensive rats" @default.
- W2898879140 doi "https://doi.org/10.1097/01.hjh.0000548045.80273.59" @default.
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