Effects of Acute Exercise on Insulin-mediated and Insulin-like Growth Factor-1-mediated Vascular Function in Spontaneously Hypertensive Rats

• Main Authors: Chien-Kuei Yeh, 葉謙魁
• Other Authors: Ai-Lun Yang
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/88735627374024349535

碩士 === 國立成功大學 === 物理治療研究所 === 97 === Background and purpose: Recent studies have indicated that insulin and insulin-like growth factor-1 (IGF-1) are important hormones that protect and regulate cardiovascular function. These two hormones can produce nitric oxide (NO) from endothelial cells, which diffuses to smooth muscle cells and induces vasorelaxation. Insulin and IGF-1 cause phosphorylation of phosphatidylinositol-3 kinase (PI3-K), activate nitric oxide synthase (NOS), and lead to NO production. Furthermore, several studies have reported that the acetylcholine (ACh)-mediated vasorelaxation is impaired in hypertension. Also, exercise has been found to improve this adverse effect. However, the effects of acute exercise on insulin-mediated and IGF-1-mediated vasorelaxation in hypertension remain unclear. Therefore, the purpose of this study was to examine the effects of acute exercise on insulin-mediated and IGF-1-mediated vascular function, as well as its underlying mechanisms, in spontaneously hypertensive rats (SHR). Methods: SHR were randomly divided into acute exercise (SHR+Ex) and sedentary groups. Age-matched Wistar-Kyoto (WKY) rats were used as control group. Single exercise intervention was conducted in the acute exercise group by running on a treadmill for sixty minutes. Immediately after exercise, the thoracic aortas of rats were isolated for the measurement of vasorelaxation. Results: We found that, (1) compared with WKY, the insulin-mediated and IGF-1-mediated vasorelaxation were significantly decreased in the SHR group; (2) acute moderate exercise significantly improved insulin-mediated and IGF-1-mediated vasorelaxation in the SHR+Ex group; (3) the alternations on insulin-mediated and IGF-1-mediated vasorelaxation were mainly caused by release of PI3-K and NOS; (4) the impairments of insulin-mediated and IGF-1-mediated vasorelaxation in SHR were associated with the increase of oxidative stress. Conclusion: Our results suggested that insulin-mediated and IGF-1-mediated vasorelaxation were impaired in hypertension, which was associated with the increase of oxidative stress. Acute moderate exercise would improve the vasorelaxation induced by insulin and IGF-1; This study provides parts of the underlying theoretical base for the improvements of hypertension-induced vascular impairment through exercise intervention.