The association between obesity and hypertension is well documented, although the exact nature of this relation remains unclear. Sympathetic nervous and renin-angiotensin-aldosterone system activation appear to play an important role in the sodium and water retention, rightward shift in the pressure-natriuresis, and blood pressure elevation observed in obese individuals. Visceral obesity and the ectopic deposition of adipose tissue may be important in the activation of these systems and in the target organ damage that ensues. Weight loss is critical in the effective management of obesity hypertension and the accompanying target organ damage, although recidivism rates are high. However, prevention of weight gain should be the major priority for combating hypertension and its consequences in the future. The present review will provide an overview of our understanding of the etiology, pathophysiology, and treatment of obesity hypertension. Our focus is on the state of knowledge in humans. The potential role of abdominal obesity is considered throughout our review. We refer to relevant animal literature for supportive evidence and where little or no data in humans are available.

We tested the hypothesis that weight loss via a hypocaloric diet would reduce arterial stiffness in overweight and obese middle-aged and older adults. Thirty-six individuals were randomly assigned to a weight loss (n=25; age: 61.2±0.8 years; body mass index: 30.0±0.6 kg/m ² ) or a control (n=11; age: 66.1±1.9 years; body mass index: 31.8±1.4 kg/m ² ) group. Arterial stiffness was measured via carotid artery ultrasonography combined with applanation tonometry and carotid-femoral pulse wave velocity via applanation tonometry at baseline and after the 12-week intervention. Body weight, body fat, abdominal adiposity, blood pressure, β-stiffness index, and carotid-femoral pulse wave velocity were similar in the 2 groups at baseline (all P >0.05). Body weight (−7.1±0.7 versus −0.7±1.1 kg), body fat, and abdominal adiposity decreased in the weight loss group but not in the control group (all P <0.05). Brachial systolic and diastolic blood pressures declined ( P <0.05) only in the weight loss group. Central systolic and pulse pressures did not change significantly in either group. β-Stiffness index (−1.24±0.22 versus 0.52±0.37 U) and carotid-femoral pulse wave velocity (−187±29 versus 15±42 cm/s) decreased in the weight loss group but not in the control group (all P <0.05). The reductions in carotid-femoral pulse wave velocity were correlated with reductions in total body and abdominal adiposity ( r =0.357–0.602; all P <0.05). However, neither total body nor abdominal adiposity independently predicted reductions in arterial stiffness indices. In summary, our findings indicate that weight loss reduces arterial stiffness in overweight/obese middle-aged and older adults, and the magnitudes of these improvements are related to the loss of total and abdominal adiposity.

We tested the hypothesis that weight gain would increase arterial stiffness in healthy nonobese adults. To address this, we overfed 14 nonobese men (age: 23±1 years) ≈1000 kcal/d for 6 to 8 weeks until a 5-kg weight gain was achieved. Carotid diameters (high-resolution ultrasound) and pressures (applanation tonometry), body composition (dual energy x-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 weeks of weight stability at each individual’s elevated body weight. Overfeeding increased body weight 5.1±0.1 kg and body fat 3.4±0.4 kg (both P <0.001) in 45±7 days. Total abdominal fat increased 46±7 cm ² with weight gain due to increases in both subcutaneous (30±6 cm ² ) and visceral fat (15±4 cm ² ; all P <0.01). As hypothesized, weight gain increased arterial stiffness 13±6% and decreased arterial compliance 21±4% (both P <0.05). Furthermore, those individuals above the median increase in abdominal visceral fat demonstrated a significantly greater increase in arterial stiffness (0.97±0.29 versus 0.06±0.36 U; P <0.05) compared with those below the median. Consistent with these observations, the only correlates of the changes in arterial stiffness with weight gain were the increases in total abdominal fat ( r =0.794), abdominal visceral fat ( r =0.651), and waist circumference ( r =0.470; all P <0.05). Taken together, these findings suggest that modest weight gain is associated with increases arterial stiffness in nonobese men. The degree of large artery stiffening with weight gain seems to be determined, in part, by the amount of abdominal visceral fat gain. Importantly, this relation is independent of the amount of total body fat gained.