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This Article Full Text Full Text (PDF) All Versions of this Article: 90/5/683    most recent expphysiol.2005.031237v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Haynes, W. G Search for Related Content PubMed PubMed Citation Articles by Haynes, W. G Related Collections Vascular Symposia Papers

¹ General Clinical Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA

Abstract

Obesity in humans causes hypertension, myocardial hypertrophy and coronary atherosclerosis, and increased cardiovascular morbidity and mortality that is thought to be related to sympathetic overactivity. Leptin is an adipocyte-derived hormone that acts in the hypothalamus to regulate appetite, energy expenditure and sympathetic nervous system outflow. One of the major mechanisms leading to the development of obesity-induced hypertension appears to be leptin-mediated sympatho-activation. Leptin adversely shifts the renal pressure–natriuresis curve, leading to relative sodium retention. Although obesity is generally associated with resistance to the anorexic and weight-reducing actions of leptin, our work has shown preservation of its sympatho-excitatory and pressor actions. This selective leptin resistance of obesity, coupled with hyperleptinaemia, may play a critical role in the cardiovascular complications of obesity. Increased information about leptin and its mechanisms of actions should help the development of safe and effective pharmacological treatments of obesity and obesity-related hypertension.

(Received 6 June 2005; accepted after revision 8 August 2005; first published online 16 August 2005)
Corresponding author W. G. Haynes: General Clinical Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA. Email: william-g-haynes{at}iowa.edu

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