Obesity, hypertension, and sympathetic nervous system activity

Abstract

Several epidemiologic studies have shown that obesity represents an independent risk factor for the development of cardiovascular diseases, including hypertension, myocardial ischemic disease, and cardiac arrhythmias. One of the most appealing concepts in obesity-related hypertension is that a specific etiology can be identified. There is now substantial evidence that human obesity is characterized by abnormalities in sympathetic cardiovascular control. The application of sensitive techniques to assess sympathetic nervous system (SNS) activity in humans, including catecholamine levels, norepinephrine (NE) spillover techniques, and microneurography have furthered this concept. Catecholamine levels in obesity have been conflicting, with high, normal, and low levels reported. However, studies examining weight loss have found that the fall in blood pressure (BP) was highly correlated with reductions in plasma NE. Examination of NE spillover in obesity has shown regional overactivity in the kidneys. High renal SNS activity could lead to sodium retention and abnormal glomerular hemodynamics that could raise BP. Microneurography, which determines muscle sympathetic outflow, has shown consistent elevation in obesity, but no difference between normotensive and hypertensive obesity. However, the hyperinsulinemia of obesity may act in concert with the SNS to elevate BP, as the combination of the two seems to produce vascular constriction. Leptin also has several cardiovascular actions that may contribute to BP regulation. Epidemiologic studies also found that SNS activity predicts hypertension in obese subjects.