Premium
Effects of long‐term aerobic exercise on vascular function mediated by insulin and insulin‐like growth factor‐1 in hypertension
Author(s) -
Chao Wen-Chia,
Yang Ai-Lun,
Su Chia-Ting,
Lin Yi-Yuan
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.866.3
Subject(s) - medicine , aerobic exercise , endocrinology , insulin , insulin receptor , insulin like growth factor , nitric oxide synthase , nitric oxide , receptor , insulin resistance , growth factor
Hypertension induces vascular dysfunction and decreases nitric oxide (NO) bioavailability. However, whether exercise influences insulin‐ and insulin‐like growth factor‐1 (IGF‐1)‐mediated vascular function in hypertension remains unclear. Thus, we aimed to investigate the effects of long‐term aerobic exercise on vascular function mediated by insulin and IGF‐1 in spontaneously hypertensive rats (SHR). Three groups of rats were used: SHR with aerobic exercise (SHR‐EX), SHR, and Wistar‐Kyoto rats (WKY) as the normotensive control group. The exercise group ran on the treadmill at moderate intensity for 1 hr/day, 5 days/week for 8 weeks. Vasorelaxant responses of rat aortas were analyzed in the organ baths. The aortic protein expression, such as insulin and IGF‐1 receptors, was also examined by Western blot. We found that, compared with the WKY, the SHR group had significantly (p<0.05) lower vasorelaxant responses to insulin and IGF‐1. However, the aerobic exercise significantly (p<0.05) improved the adverse effects in the SHR‐EX group. After treating the inhibitors of NO synthase and phosphatidylinositol‐3 kinase (PI3K), the differences of vascular responses among three groups were eliminated. In addition, the protein expression of insulin and IGF‐1 receptors was significantly (p<0.05) increased in the SHR‐EX group. Our results suggested that long‐term aerobic exercise ameliorated hypertension‐induced vascular dysfunction mediated by insulin and IGF‐1.