Effects of acute severe exercise on insulin‐ and insulin‐like growth factor‐1‐mediated vasorelaxation in spontaneously hypertensive rats

Abstract

Exercise enhances the vascular function mainly by improving endothelial function. The way of exercise influences on hypertension‐induced vascular dysfunction remains unclear. Thus, the aim of this study was to examine the effects of acute severe exercise on insulin‐ and insulin‐like growth factor‐1 (IGF‐1)‐mediated vasorelaxation in spontaneously hypertensive rats (SHR). Three groups of rats were used in this study: SHR with exercise, SHR, and Wistar‐Kyoto rats (WKY) as control. The SHR with acute severe exercise group ran on treadmill at the speed of 28‐30 m/min until exhausted. Thoracic aortas were isolated to analyze vascular responses in organ baths. Selective inhibitors were used to examine the roles of endothelial nitric oxide synthase (eNOS) and phosphatidylinositol‐3 kinase (PI3K) in the vasorelaxation. Furthermore, the vascular response induced by sodium nitroprusside (SNP, a NO donor) was examined. Our results showed that, 1) insulin‐ and IGF‐1‐mediated vasorelaxation was significantly lower in SHR than WKY; 2) acute exercise ameliorated these adverse effects in SHR; 3) after treating either wortmannin (a PI3K inhibitor) or L‐NAME (a eNOS inhibitor), the differences of vascular responses among three groups were eliminated; 4) no significant differences of the SNP‐induced vasorelaxation were found among three groups. Our findings suggested that acute severe exercise could reverse the impairments of vascular function in hypertension.