Obesity, Sympathetic Overdrive, and Hypertension

Abstract

If not reversed, the steady rise in overweight and obesity is expected to become the leading cause of death and to outweigh the health benefits resulting from improved therapies and cardiovascular risk management and continued reductions in the prevalence of behavioral risk factors, such as smoking.1 Indeed, obese patients often develop diabetes mellitus and have increased cardiovascular risk factors, including hypertension. The discovery of the adipocyte-derived hormone leptin brought a new perspective to the pathophysiological mechanisms of obesity and associated diseases. Initial studies of leptin showed that it regulates appetite and enhances energy expenditure by activating sympathetic nerve activity to thermogenic brown adipose tissue. Additional studies demonstrated that leptin also causes sympathetic excitation to the kidney that, in turn, increases arterial pressure.2 Prior et al,3 in the present issue of Hypertension , provide compelling evidence implicating leptin in obesity-associated cardiovascular adverse effects. These authors first performed a longitudinal analysis of the hemodynamic parameters and sympathetic tone in diet-induced obese rabbits. Importantly, sympathetic nerve activity was assessed using several approaches, including multifiber recording in the conscious state. As expected, the development of obesity was associated with an increase in arterial pressure and heart rate. The obese rabbits also exhibited higher sympathetic tone, as indicated by the elevated plasma catecholamines and renal sympathetic nerve activity. These data demonstrate a close relationship among excessive adiposity, hypertension, and overactivity of renal sympathetic nerves. Overactivity of the sympathetic nervous system is a common feature of obesity in humans. Study of regional sympathetic activity in obese humans using …