Mechanisms in obesity-related hypertension: role of insulin and catecholamines.

Although the association of obesity and hypertension is well recognized, the mechanisms involved in the pathogenesis of increased blood pressure in the obese are poorly understood. Recent studies addressing the impact of 1) body fat distribution on blood pressure and 2) dietary intake on sympathetic nervous system (SNS) activity suggest a plausible hypothesis that relates the hypertension of the obese to hyperinsulinemia and SNS stimulation. Hypertension in the obese is associated with fat accumulation in the upper body segments; this type of obesity is also characterized by hyperinsulinemia and insulin resistance. Insulin, moreover, is an important signal in the relationship between dietary intake and SNS activity: increased insulin levels are associated with SNS stimulation. The hyperinsulinemia of obesity may, therefore, increase blood pressure by 1) direct effects of insulin to stimulate renal sodium reabsorption, and 2) sympathetic stimulation of the heart, blood vessels, and kidney. Conversely, SNS suppression and diminished insulin following caloric restriction may explain the hypotensive effects of caloric restriction in obese hypertensive subjects. The hypothesis presented here emphasizes the important role of diet in the treatment of obese hypertensive subjects. The efficacy of caloric restriction, weight loss, and exercise in reducing blood pressure in the obese is linked to diminished insulin and SNS activity and may be viewed as evidence in favor of this hypothesis.