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25‐Hydroxyvitamin D deficiency is associated with vascular endothelial dysfunction in middle‐aged and older adults
Author(s) -
Jablonski Kristen L,
Pierce Gary L,
Walker Ashley E,
Chonchol Michel,
Seals Douglas R
Publication year - 2010
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.24.1_supplement.1039.7
Subject(s) - medicine , brachial artery , endothelial dysfunction , vitamin d and neurology , vitamin d deficiency , endothelium , oxidative stress , endocrinology , blood pressure
Aging is associated with impaired endothelium‐dependent dilation (EDD) and increased 25‐hydroxyvitamin D (25(OH)D) deficiency. 25(OH)D deficiency is predictive of incident cardiovascular events and mortality. We hypothesized that healthy middle‐aged and older adults (MA/O) who were 25(OH)D insufficient (20–29 ng/mL) or deficient (<20 ng/mL) would demonstrate greater impairment in EDD compared with their 25(OH)D sufficient (>30 ng/mL) peers. Groups did not differ in cardiovascular risk factors or physical activity/fitness. EDD, measured using brachial artery flow‐mediated dilation (FMD), was 25% and 42% lower in insufficient (63±1 yr, n=24, mean±S.E.) and deficient (64±1 yr, n=14) vs. sufficient (60±2 yr, n=8) subjects (3.0±0.3 vs. 3.9±0.3 vs. 5.2±0.5 %, p<0.01), whereas endothelium‐independent dilation (brachial dilation to sublingual nitroglycerine) did not differ among groups (p=0.30). In the overall sample, 25(OH)D was positively related to FMD (r= 0.50; p<0.01) and inversely related to vascular endothelial cell nitrotryosine, a marker of oxidative damage (n=24; r=−0.63; p<0.01). These results indicate that lower circulating 25(OH)D may contribute to oxidative stress‐associated impairment of EDD among healthy MA/O, and suggest vitamin D supplementation may improve EDD in this group. NIH AG013038 , AG022241 , AG006537 , AG0015897, AG03114, AG033994 , RR00051