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BACKGROUND The relationship between pediatric severe obesity (SO) and central aortic blood pressure (BP) has yet to be established. METHODS We conducted a cross-sectional study of 348 youth (48.5% male, age 12.7 ± 0.1 years) with a wide range of body mass index (BMI) values: normal weight (NW; ≥5th and RESULTS After adjustment for covariates, no significant sex differences were observed for radial−aortic systolic blood pressure (SBP) (P = 0.39), carotid−aortic SBP (P = 0.99), radial−aortic diastolic blood pressure (DBP) (P = 0.44), and carotid−aortic DBP (P = 0.53). Compared to youth with NW, youth with SO exhibited higher radial−aortic SBP (SO vs. NW: 102 ± 1 mm Hg vs. 90 ± 1 mm Hg, P CONCLUSIONS In a cohort of youth with a wide range of adiposity levels, central aortic BP was elevated among individuals with SO and associated with BMI but not body fatness.

The independent and combined effects of aerobic exercise training (AEX) and weight loss (WL) on blood pressure (BP) and oral glucose tolerance were studied in 97 nondiabetic, sedentary, older men. The men were assigned to either a WL (n = 31), AEX (n = 35), AEX+WL (n = 20) intervention, or to a control (CON) group (n = 11). The AEX regimen consisted of 3 days/week for 9 months, whereas WL consisted of a behavioral modification weight loss program that met weekly for 9 months. Maximal oxygen uptake increased significantly (P < .05) in both the AEX and AEX+WL groups (delta change: 0.45 +/- 0.06 and 0.43 +/- 0.07 L/min, respectively; mean +/- SEM), but did not change in the WL (delta change: 0.00 +/- 0.04 L/min) and CON (-0.05 +/- 0.07 L/min) groups. The AEX+WL and WL groups had comparable reductions in body weight (-8.6 +/- 0.7 and -8.8 +/- 0.7 kg,) and %fat (-5.4 +/- 0.5 and -5.2 +/- 0.6%) that were significantly greater than the CON and AEX groups, in which neither body weight nor %fat changed. The AEX, WL, and AEX+WL groups had significant reductions in both systolic (-6.4 +/- 1.3, -9.2 +/- 1.6, and -9.7 +/- 2.2 mm Hg, respectively) and diastolic (-5.2 +/- 1.0, -6.2 +/- 1.3, and -7.2 +/- 1.5 mm Hg, respectively) BP after their respective interventions compared with the change in systolic (3.2 +/- 3.6 mm Hg) and diastolic (-0.5 +/- 1.9 mm Hg) BP in the CON group. The AEX, WL, and AEX+WL groups also had significant reductions in glucose and insulin responses to an oral glucose tolerance test compared with the CON group. The reduction in the insulin area in the AEX+WL group was significantly greater than in the AEX and WL groups. The results of this study demonstrate that AEX and WL are effective nonpharmacologic therapies to lower BP and alter glucose and insulin responses to an oral glucose challenge. However, combining the two interventions does not result in any further improvement in BP.

Individuals differ in their blood pressure (BP) response to changes in dietary sodium (Na+) intake. It is possible that differences in BP responses to dietary Na+ are influenced by genes.A total of 35 older (62.9 +/- 1.2 years) hypertensive subjects had their mean arterial blood pressure (MABP) determined after 8 days of low (20 mmol/day) and high (200 mmol/day) Na+ intake. The insertion/ deletion polymorphism of the angiotensin converting enzyme (ACE) gene was genotyped with standard polymerase chain reaction methods.Of the 35 subjects, 24 were classified as sodium-sensitive (or = 5 mm Hg increase in MABP in response to the increase in dietary Na+) and 11 were classified as sodium-resistant (5 mm Hg increase in MABP). Those homozygous for the insertion allele of the ACE gene (insertion/insertion [II]; n = 8) had lower (P = .04) MABP responses to the increase in dietary Na+ (0 +/- 3 mm Hg) compared to heterozygotes (insertion/deletion [ID]; n = 20) (9 +/- 2 mm Hg; P = .0001) and those homozygous for the deletion allele (deletion/deletion [DD]; n = 7) (9 +/- 3 mm Hg; P = .05). The prevalence of sodium sensitivity was higher (P = .0083) in DD (71%) and ID (83%) compared to II (25%) genotype groups.Based on these data in older hypertensive individuals, we conclude that the ACE gene ID and DD genotypes are associated with an increase in BP during a high Na+ diet, which is consistent with the phenotypic characteristic of sodium sensitivity.

The majority of older hypertensive humans are sodium sensitive and they are characterized by increased alpha-adrenergic responsiveness relative to their level of sympathetic nervous system (SNS) activity. To test the hypothesis that heightened SNS activity and/or increased alpha-adrenergic receptor responsiveness during sodium loading may play a role in the sodium-dependent increase in blood pressure in older sodium-sensitive hypertensives, we used compartmental analysis of [3H]norepinephrine (NE) kinetics to determine the release rate of NE into an extravascular compartment (NE2) as an index of systemic SNS activity and determined forearm blood flow responses to graded intrabrachial artery NE and angiotensin II (ANG II) infusions and platelet membrane alpha2-receptor properties in 24 older (age 64 +/- 7 years) hypertensive subjects. Subjects were studied at the end of 1 week of a low (20 mmol/day)- and again at the end of 1 week of a high (200 mmol/day)-sodium diet. Subjects were categorized as sodium sensitive (SS) if they had a > or = 5 mm Hg increase in mean arterial blood pressure (MABP) with dietary sodium loading (n = 16), or sodium-resistant (SR) if their MABP increased by < 5 mm Hg (n = 8). Neither dietary sodium intake nor sodium-sensitivity status significantly affected arterial plasma NE levels, NE2, or other NE kinetic parameters. Forearm blood flow responses to NE or to ANG II, and platelet alpha2-receptor properties were similar between the SS and SR groups. These results suggest that the sodium-dependent increase in MABP that characterizes SS hypertension among older humans is not because of an increase in systemic SNS activity or increased arterial adrenergic receptor responsiveness.

We sought to determine whether reductions in blood pressure in hypertensives after acute exercise persist for more than the 2 to 3 h found in controlled laboratory settings. Subjects (n = 11) were obese (32 ± 4% body fat), sedentary (VO 2max 27 ± 4 mL/kg/min) 60 ± 6-year-old men with stage 1 or 2 essential hypertension. Ambulatory blood pressure was recorded on 1 day preceded by 45 min of 70% VO 2max treadmill exercise and on another day not preceded by exercise. Systolic blood pressure was lower by 6 to 13 mm Hg for the first 16 h after exercise ( P .05) compared to the day without prior exercise. Twenty-four-hour, day, and night average systolic blood pressures were significantly lower on the day after exercise. There was a trend for peak systolic blood pressure to be lower during the entire 24 h and the day portion of the recording; peak systolic blood pressure was significantly lower during the night portion of the recording after exercise. Systolic blood pressure load (percent of systolic blood pressure readings > 140 mm Hg) was reduced during the entire 24 h and the day portion of the recording after exercise. Diastolic blood pressure was lower for 12 of the first 16 h after acute exercise (hours 0 to 4, 5 to 8, 13 to 16) ( P .05) compared to the day without prior exercise. Twenty-four-hour, day, and night average diastolic blood pressure was also significantly lower on the recording after exercise. Peak diastolic blood pressure was lower over the entire 24-h period. Diastolic blood pressure load (percent of diastolic blood pressure readings > 90 mm Hg) was lower during the entire 24 h and the day portion of the day after exercise. Preliminary data also suggest that common genetic polymorphisms at the angiotensinogen, lipoprotein lipase, and angiotensin converting enzyme loci may affect the blood pressure-lowering response after acute exercise. Thus, in sedentary, obese hypertensive men a single aerobic exercise session reduced blood pressure enough to result in significantly lower 24-h average systolic, diastolic, and mean arterial blood pressure. This could result in a reduced cardiovascular load during the 24 h after acute exercise in older hypertensive men.

Elevated levels of circulating soluble cell adhesion molecules are associated with the development of cardiovascular disease. We tested the hypothesis that circulating levels of soluble cell adhesion molecules are elevated in older men with uncomplicated essential hypertension, which may contribute to the increased risk of atherosclerosis in this population. Circulating levels of soluble intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin were measured in 11 hypertensive (69+/-1 years) and ten normotensive (65+/-1 years) older men who were free of overt atherosclerotic disease, diabetes, and dyslipidemia. The hypertensive subjects had higher (P.05) circulating levels of soluble intercellular adhesion molecule-1 (232.4+/-16.5 v 189.8+/-11.1 ng/mL) and vascular adhesion molecule-1 (737.3+/-65.6 v 565.7+/-46.8 ng/mL) compared with their normotensive peers. However, there was no difference in the levels of soluble E-selectin between the hypertensive (51.1+/-3.9 ng/ mL) and normotensive (48.8+/-6.6 ng/mL) subjects. Univariate analysis revealed a positive correlation between soluble intercellular adhesion molecule-1 and both systolic (r = 0.50, P = .02) and diastolic (r = 0.49, P = .03) blood pressure. In addition, soluble vascular adhesion molecule-1 was positively correlated with age (r = 0.60, P = .004) and systolic blood pressure (r = 0.43, P = .05). The results of this study support the hypothesis that circulating levels of soluble cell adhesion molecules are elevated in older men with uncomplicated essential hypertension.

Increased dietary sodium intake has been associated with an increase in blood pressure as well as a decrease in insulin-mediated glucose disposal in young healthy adults. The purpose of this study was to determine whether dietary sodium intake is associated with changes in oral glucose tolerance, insulin sensitivity, and blood pressure in older, sedentary, overweight hypertensives. Eight older (70.0 +/- 1.4 years, mean +/- SEM), overweight (40.2 +/- 3.1% body fat), mildly hypertensive (151 +/- 8/82 +/- 2 mm Hg) patients with a fasting plasma glucose7.8 mmol/L were studied after 2 weeks on low (3 g/day) and 2 weeks on high (10 g/day) sodium diets. To examine carbohydrate metabolism we performed a 2 h oral glucose tolerance test and a two-dose (240 and 600 pmol/m2/min) hyperinsulinemic-euglycemic clamp at the end of each sodium diet. High sodium intake was associated with a significantly greater urinary sodium excretion (364 +/- 45 mmol/day v 112 +/- 21 mmol/day; P.0001). The increase in dietary sodium from low to high did not result in significant differences in fasting plasma glucose (6.0 +/- 0.2 v 5.8 +/- 0.1 mmol/L, P = .20) or insulin (72.5 +/- 7.8 v 69.9 +/- 12.4 pmol/L, P = 0.71) levels or in the glucose (374.0 +/- 50.8 v 493.2 +/- 45.0 mmol/min/L, P = .12) and insulin (43,783 +/- 10,278 v 44,110 +/- 12,392 pmol/min/L, P = .96) areas determined during the oral glucose tolerance test. Similarly, there was no effect of dietary sodium on insulin-mediated glucose disposal at low (5.87 +/- 1.02 v 5.60 +/- 0.94 mg/kgLBM/min, P = .36) or high (12.15 +/- 1.49 v 11.91 +/- 1.49 mg/kgLBM/min, P = .64) insulin infusion rates. Our findings suggest that, in insulin resistant hypertensives, increased dietary sodium does not affect either glucose or insulin responses during an oral glucose tolerance test or glucose disposal during a hyperinsulinemic euglycemic clamp.