Voluntary Wheel Running Attenuates Salt-Induced Vascular Stiffness Independent of Blood Pressure

自愿跑轮运动可减轻盐诱导的血管僵硬,且与血压无关

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作者:John J Guers, William B Farquhar, David G Edwards, Shannon L Lennon

Background

Excess dietary salt can lead to the development of arterial stiffness and high blood pressure (BP). Regular physical activity can protect against arterial stiffening and lower BP. Less is known regarding the role of exercise on the vasculature independent of BP under high salt (HS) conditions. The

Conclusions

These data suggest that VWR may protect against collagen accumulation through a TGF-β-mediated pathway by improving nitric oxide bioavailability and redox balance in rats.

Methods

Rats were maintained on either normal salt (NS; 0.49% NaCl) or HS (4.0% NaCl) diet for 6 weeks and further divided into a voluntary wheel running (NS-VWR, HS-VWR) or cage control group (NS, HS). Carotid-femoral pulse wave velocity (PWV) was measured using applanation tonometry at baseline (BSL) and 6 weeks.

Results

BP was measured weekly and remained unchanged among groups throughout the 6 weeks (P > 0.05). PWV was elevated at 6 weeks in HS compared to baseline (HS-BSL, 3.27 ± 0.17 vs. HS-6 week, 4.13 ± 0.26 m/s; P < 0.05) and was lower at 6 weeks in both VWR groups (NS-VWR, 2.98 ± 0.29, HS-VWR, 3.11 ± 0.23 m/s) when compared to HS at 6 weeks (P < 0.05). This was supported by a significant increase in aortic collagen I in the HS group alone and transforming growth factor beta (TGF-β) was greater in the HS group compared to both NS groups (P < 0.05). Wheel running resulted in a greater aortic phosphorylated eNOS and SOD-2 in HS-WVR (P < 0.05) compared to HS. Conclusions: These data suggest that VWR may protect against collagen accumulation through a TGF-β-mediated pathway by improving nitric oxide bioavailability and redox balance in rats.

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