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(Hypertension. 2008;51:168.)
© 2008 American Heart Association, Inc.

Hypertension Highlights

Should We Target the Sympathetic Nervous System in the Treatment of Obesity-Associated Hypertension?

From the Department of Medicine and Pharmacology, Division of Clinical Pharmacology, and the Autonomic Dysfunction Center, Vanderbilt University School of Medicine, Nashville, Tenn.

Correspondence to Italo Biaggioni, 556 RRB, Vanderbilt University, Nashville, TN 37232. E-mail Italo.biaggioni@vanderbilt.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
An estimated 60% to 70% of hypertension may be attributed to obesity.¹ As our population increases in weight and girth, obesity-associated hypertension will be an increasing medical problem, contributing to greater health care costs and reversing the gains that we have achieved in the treatment of hypertension. Considering that 30% of hypertensive subjects are undiagnosed, 40% remain untreated, and, of those being treated, 65% do not meet treatment goals,² the opening of the spigot of obesity-associated hypertension will result in an ever-growing number of patients with uncontrolled hypertension, particularly because obesity is a predictor of poor blood pressure control.³ It is important, therefore, to understand the pathophysiology of obesity-associated hypertension. This commentary focuses on the role that the sympathetic nervous system plays in this condition and its relevance to treatment.

	Sympathetic Activity and Obesity-Associated Hypertension

 
Landsberg⁴ postulated that obesity induces sympathetic activation as a compensatory mechanism to increase resting energy expenditure and restore energy balance; sympathetically mediated hypertension is the price to pay for this beneficial metabolic effect. A competing MONA LISA (Most Obesities kNown Are Low In Sympathetic Activity) hypothesis postulates that lower sympathetic activity is an initiating event leading to decreased energy expenditure and obesity.⁵ In white populations, in whom most of the studies have been done, the preponderance of evidence supports the concept that sympathetic activation accompanies obesity-associated hypertension. There is less agreement about the cause of sympathetic activation; potential culprits include the increase in insulin, leptin, and angiotensin II; the decrease of adiponectin; and the sleep apnea^6,7 associated with obesity. Despite . . . [Full Text of this Article]

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