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Vasodilatory Function in Human Skeletal Muscle Arteries with Advancing Age: Role of Adropin
Author(s) -
Kwon Oh Sung,
Andtbacka Robert,
Hyngstrom John,
Richardson Russell
Publication year - 2017
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.31.1_supplement.684.2
Subject(s) - vasodilation , electrical impedance myography , sodium nitroprusside , medicine , endocrinology , endothelial dysfunction , acetylcholine , skeletal muscle , endothelium , middle age , nitric oxide , vascular smooth muscle , smooth muscle
Background Aging is associated with impaired endothelium‐dependent dilation in human skeletal muscle feed arteries (SMFAs). However, the specific mechanisms underlying the age‐related impairment in the regulation of blood flow have yet to be clarified. Recent evidence has suggested that adropin, a peptide secreted by the liver, may play a role in cardiovascular health. Therefore, this study sought to determine if treatment with adropin, in vitro , can restore the age‐related endothelial dysfunction in human SMFAs. Methods Adropin protein expression was assessed in 3 groups of subjects, young (28±4 yrs, n=10), middle aged (50±6 yrs, n=10) and old (75±7 yrs, n=16) with Western blot analysis. Using pressure myography, vasodilation in SMFAs with and without adropin incubation, from these young, middle aged, and old subjects was assessed in response to three stimuli 1) flow‐induced shear stress, 2) acetylcholine (ACh), and 3) sodium nitroprusside (SNP). Results Progressive age‐related reductions in endothelial‐dependent vasodilatory function were evident in response to both flow (Young: 97 ± 13; Middle‐age: 62 ± 12; Old: 32 ± 14%, P < 0.05) and ACh (Young: 98 ± 15, Middle‐age: 68 ± 13 %; Old: 40 ± 10 %, P < 0.05). Adropin treatment in the middle aged and old SMFAs restored the vasodilatory response to flow (Middle‐age + Adropin: 88 ± 10; Old + Adropin: 78 ± 11 %) and ACh (Middle‐age + Adropin: 94 ± 16%; Old + Adropin: 83 ± 10 %, P < 0.05) ( p <0.05). Endothelium‐independent vasodilation (SNP) was unaffected by age and adropin, also, had no effect. Interestingly, adropin upregulated eNOS protein expression in the middle aged and old SMFAS and there was a significant positive correlation between adropin protein expression and both flow‐mediated and ACh‐dependent vasodilation. Conclusions Overall, these findings suggest that adropin may play a critical role in age‐associated endothelial dysfunction. Furthermore, adropin could be a novel therapeutic approach to restore endothelial function and NO bioavailability in the elderly. Support or Funding Information NIH Heart, Lung, Blood Institute grants (HL‐ 091830) and Veterans Affairs Rehabilitation Research and Development Merit (E6910‐R)