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The degree of arterial dilatation induced by exogenous nitrates (nitrate-mediated dilatation, NMD) has been similar in obese and normal-weight adults after single high-dose glyceryl trinitrate (GTN). We examined whether NMD is impaired in obesity by performing a GTN dose-response study, as this is a potentially more sensitive measure of arterial smooth muscle function. In this cross-sectional study, subjects were 19 obese (age 31.0 ± 1.2 years, 10 male, BMI 44.1 ± 2.1) and 19 age- and sex-matched normal-weight (BMI 22.4 ± 0.4) young adults. Blood pressure (BP), triglycerides, high-density lipoprotein (HDL), and low-density lipoprotein (LDL)-cholesterol, glucose, insulin, high-sensitivity C-reactive protein (hs-CRP), carotid intima-media thickness (CIMT), and flow-mediated dilatation (FMD) were measured. After incremental doses of GTN, brachial artery maximal percent dilatation (maximal NMD) and the area under the dose-response curve (NMD AUC) were calculated. Maximal NMD (13.4 ± 0.9% vs. 18.3 ± 1.1%, P = 0.002) and NMD AUC (54,316 ± 362 vs. 55,613 ± 375, P = 0.018) were lower in obese subjects. The obese had significantly higher hs-CRP, insulin, and CIMT and lower HDL-cholesterol. Significant bivariate associations existed between maximal NMD or NMD AUC and BMI-group (r = -0.492, P = 0.001 or r = -0.383, P = 0.009), hs-CRP (r = -0.419, P = 0.004 or r = -0.351, P = 0.015), and HDL-cholesterol (r = 0.374, P = 0.01 or r = 0.270, P = 0.05). On multivariate analysis, higher BMI-group remained as the only significant determinant of maximal NMD (r² = 0.242, β = -0.492, P = 0.002) and NMD AUC (r² = 0.147, β = -0.383, P = 0.023). In conclusion, arterial smooth muscle function is significantly impaired in the obese. This may be important in their increased cardiovascular risk.

As humans spend a significant amount of time in the postprandial state, we examined whether vascular reactivity (a key indicator of cardiovascular health) was different after a high-fat meal in 11 obese (median BMI 46.4, age 32.1 +/- 6.3 years, 7 men) and 11 normal weight (median BMI 22.6) age- and sex-matched controls. At baseline and 1 and 3 h postmeal, blood pressure (BP), heart rate (HR), reactive hyperemia peripheral artery tonometry (RH-PAT) index, radial augmentation index adjusted for HR (AIx75), brachial pulse wave velocity (PWV(b)), glucose, insulin, total and high-density lipoprotein (HDL) cholesterol, and triglycerides were measured. Brachial flow-mediated dilatation (FMD) and, by venous plethysmography, resting and hyperemic forearm blood flows (FBFs) were measured at baseline and 3 h. At baseline, obese subjects had higher systolic BP, HR, resting FBF, insulin and equivalent FMD, RH-PAT, hyperemic FBF, AIx75, PWV(b), glucose, total cholesterol, triglycerides, and lower HDL cholesterol. In obese and lean subjects, FMD at baseline and 3 h was not significantly different (6.2 +/- 1.7 to 5.8 +/- 4.3% for obese and 4.7 +/- 4.1 to 4.3 +/- 3.9% for normal weight, P = 0.975 for group x time). The meal did not produce significant changes in RH-PAT, hyperemic FBF, and PWV(b) in either group (P > 0.1 for the effect of time and for group x time interactions). In conclusion, the vascular responses to a high-fat meal are similar in obese and normal weight young adults. An exaggerated alteration in postprandial vascular reactivity is thus unlikely to contribute importantly to the increased cardiovascular risk of obesity.