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(Hypertension. 2006;48:787.)
© 2006 American Heart Association, Inc.

Brief Reviews

Mechanisms of Sympathetic Activation in Obesity-Related Hypertension

Murray Esler; Nora Straznicky; Nina Eikelis; Kazuko Masuo; Gavin Lambert; Elisabeth Lambert

From the Human Neurotransmitter Laboratory, Baker Heart Research Institute, Melbourne, Australia.

Correspondence to Murray Esler, Baker Heart Research Institute, PO Box 6492 St Kilda Rd Central, Melbourne, Victoria 8008, Australia. E-mail murray.esler@baker.edu.au

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

	Introduction

 
Obesity prevalence is soaring in industrialized countries and progressively increasing in the developing world. Altered patterns of nutrition and reduction in work-related energy expenditure have led to obesity becoming a truly global health issue. The central thermodynamic formulation for the origins of obesity, a mismatched energy balance equation, with an excess of dietary calorie intake over body energy expenditure, is a first step in the understanding of this phenomenon but leaves the diverse causal issues unexplored.

Dietary calorie intake is modified by multiple social, economic, and cultural issues. Similarly, the reduction in energy expenditure in recent decades has complex origins, deriving from demographic and social change, which includes third-world transition from a labor-intensive agricultural economy to an industrial base, the introduction of household labor-saving devices, the popularity of transportation modes not reliant on physical effort, and from changed recreational habits, particularly in childhood (computer games instead of physical games). The prevalence of childhood obesity is escalating, having whimsically but not entirely unrealistically been attributed to "potato chips and computer chips."

Obesity and hypertension are intimately associated, and both very commonly coexist in individual patients with insulin resistance, hyperinsulinemia, and hyperlipidemia, this clustering of adverse health factors¹ being designated the metabolic syndrome. The pathophysiological mechanisms by which obesity leads to hypertension remain uncertain. Understanding these processes might, perhaps, provide a more rational basis for drug treatment of obesity-related hypertension. Attempts at reduction in body weight, although pivotal in the treatment of obesity-related hypertension, more often than not fail, so that antihypertensive . . . [Full Text of this Article]

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