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We tested the hypothesis that vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults. In 127 men and women aged 48-77 yr, brachial artery flow-mediated dilation (FMD) was positively related to dietary niacin intake [%change (Δ): r = 0.20, P < 0.05; mmΔ: r = 0.25, P < 0.01]. In subjects with above-average dietary niacin intake (≥22 mg/day, NHANES III), FMD was 25% greater than in subjects with below-average intake (P < 0.05). Stepwise linear regression revealed that dietary niacin intake (above vs. below average) was an independent predictor of FMD (%Δ: β = 1.8; mmΔ: β = 0.05, both P < 0.05). Plasma oxidized low-density lipoprotein, a marker of systemic oxidative stress, was inversely related to niacin intake (r = -0.23, P < 0.05) and was lower in subjects with above- vs. below-average niacin intake (48 ± 2 vs. 57 ± 2 mg/dl, P < 0.01). Intravenous infusion of the antioxidant vitamin C improved brachial FMD in subjects with below-average niacin intake (P < 0.001, n = 33), but not above-average (P > 0.05, n = 20). In endothelial cells sampled from the brachial artery of a subgroup, dietary niacin intake was inversely related to nitrotyrosine, a marker of peroxynitrite-mediated oxidative damage (r = -0.30, P < 0.05, n = 55), and expression of the prooxidant enzyme, NADPH oxidase (r = -0.44, P < 0.01, n = 37), and these markers were lower in subjects with above- vs. below-average niacin intake [nitrotyrosine: 0.39 ± 0.05 vs. 0.56 ± 0.07; NADPH oxidase: 0.38 ± 0.05 vs. 0.53 ± 0.05 (ratio to human umbilical vein endothelial cell control), both P < 0.05]. Our findings support the hypothesis that higher dietary niacin intake is associated with greater vascular endothelial function related to lower systemic and vascular oxidative stress among healthy middle-aged and older adults. [ABSTRACT FROM AUTHOR]

In the present study, we tested the hypothesis that age-associated vascular endothelial dysfunction is exacerbated by IFG (impaired fasting plasma glucose) and that regular aerobic exercise prevents this effect. Data were analysed from a cohort of 131 non-smoking men and women without overt clinical disease. Compared with young adult controls (age=24± 1 years, n=29; values are means± S.E.M.), brachial artery FMD (flow-mediated dilation), a measure of conduit artery EDD (endothelium-dependent dilation), was 33% lower [7.93± 0.33 against 5.27± 0.37%? (% change), P<0.05] in MA/O (middle-aged/older) adults with NFG (normal fasting plasma glucose) (=99 mg/dl, 62± 1 years, n=35). In MA/O adults with IFG (100-125 mg/dl, 64± 1 years, n=28), FMD was 30% lower (3.37± 0.35%?) than in their peers with NFG and 58% lower than young controls (P<0.05). Brachial artery FMD was greater (6.38± 0.35%?) in MA/O adults with NFG who regularly performed aerobic exercise (>45 min/day for =5 days/week, 62± 1 years, n=23) compared with their non-exercising peers and only slightly less than young controls (P<0.05). Most importantly, FMD was completely preserved in MA/O adults with IFG who regularly performed aerobic exercise (6.99± 0.69%?, 65± 1 years, n=16). In the pooled sample, fasting plasma glucose was inversely related to FMD (r= -0.42, P<0.01) and was the strongest independent predictor of FMD (R2 =0.32). Group differences in FMD were not affected by other subject characteristics or brachial artery properties, including brachial artery dilation to sublingual NTG (nitroglycerine, i.e. endothelium-independent dilation). IFG exacerbates age-associated vascular endothelial dysfunction and this adverse effect is completely prevented in MA/O adults who regularly perform aerobic exercise. [ABSTRACT FROM AUTHOR]

The article discusses a study which investigated the effectiveness of fenofibrate in improving endothelium-dependent dilation in middle-aged and older normolipidemic adults by lessening oxidative stress. The study involved 24 healthy middle-aged and older men and women. It was found that short-term treatment with fenofibrate improved vascular endothelial function in the human subjects.

We tested the hypothesis that reductions in vascular endothelial function (endothelium-dependent dilation, EDD) with age are related to increases in sympathetic activity. Among 314 healthy men and women, age was inversely related to brachial artery flow-mediated dilation (FMD) (r = -0.30, P < 0.001), a measure of EDD, and positively related to plasma norepinephrine concentrations (PNE), a marker of sympathetic activity (r = 0.49, P < 0.001). Brachial FMD was inversely related to PNE in all subjects (r = -0.25, P < 0.001) and in men (n = 187, r = -0.17, P = 0.02) and women (n = 127, r = -0.37, P < 0.001) separately. After controlling for PNE (multiple regression analysis), brachial FMD remained significantly related to age in all subjects (r = -0.20, P < 0.001) and in men (r = -0.23, P < 0.01), but not women (r = -0.16, P = 0.06). Consistent with this, brachial FMD remained significantly related to PNE when controlling for age (r = -0.24, P < 0.01) and menopause status (r = -0.24, P < 0.01) in women. Indeed, PNE was the strongest independent correlate of brachial FMD in women after controlling for conventional cardiovascular disease risk factors (r = -0.22, P = 0.01). This relation persisted in a subset of women (n = 113) after further accounting for the effects of plasma oxidized low-density lipoprotein (P < 0.05), a circulating marker of oxidative stress. Endothelium-independent dilation was not related to age in either men or women (P > 0.05). These results provide the first evidence that EDD is inversely related to sympathetic activity, as assessed by PNE, among healthy adults varying in age. In particular, our findings suggest that sympathetic nervous system activity may be a key factor involved in the modulation of vascular endothelial function with aging in women. [ABSTRACT FROM AUTHOR]