| Summary: | 碩士 === 國立成功大學 === 物理治療研究所 === 97 === Background and Purpose: Insulin and insulin-like growth factor-1 (IGF-1) play important roles in the regulation of vascular tone via producing endothelium-derived nitric oxide (EDNO). Previous studies have demonstrated the impairments of endothelium-dependent vasorelaxation in hypertension. Furthermore, exercise is well known to improve vascular function through enhancing NO bioavailability. However, the effects of high-intensity exercise on insulin- and IGF-1-mediated vasorelaxation in
hypertension remain unknown. Therefore, the aim of this study was to investigate the effects of high-intensity exercise on vasorelaxant responses to insulin and IGF-1 in spontaneously hypertensive rats (SHR) and the underlying mechanisms.
Methods: Three groups of rats were used in this study: SHR with high-intensity exercise (SHR+Ex), sedentary SHR (SHR),
and Wistar-Kyoto rat (WKY) groups. The SHR+Ex group ran on treadmill at the speed of 28-30 m/min until exhaustion. The WKY group was used as normotensive control group. After high-intensity exercise, the thoracic aortas of rats were isolated immediately to measure insulin- and IGF-1-mediated vascular responses. Selective inhibitors were used to examine the roles of nitric oxide synthase (NOS) and phosphatidylinositol-3 kinase (PI3-K) in the vasorelaxation. The vascular response induced by sodium nitroprusside (SNP, a NO donor) was also examined. Finally, superoxide dismutase (SOD), a superoxide scavenger, was used to evaluate the role of superoxide production in the vasorelaxation.
Results: We found that, 1) insulin- and IGF-1-mediated
vasorelaxation was significantly reduced in SHR compared with that in WKY; 2) high-intensity exercise ameliorated these adverse effects in SHR+Ex group; 3) the alterations of vascular responses to insulin and IGF-1 were mainly due
to the varied activities of PI3-K and NOS; 4) SNP-induced,
endothelium-independent vasorelaxation was comparable among three groups; 5) the exercise-induced beneficial effects on vascular dysfunction in hypertension could be related to the reduced level of superoxide production.
Conclusions: Our findings suggested that high-intensity exercise ameliorated the hypertension-induced vascular dysfunction through the endothelium-dependent PI3-K-NOS pathway, which was associated with the reduced level of superoxide production. This study supports the effectiveness of exercise intervention in reversing vascular dysfunction in hypertension.
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