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(Hypertension. 1999;33:537-541.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the Specialized Center of Research in Hypertension and Cardiovascular Center, Department of Internal Medicine, University of Iowa, and Veterans Administration Medical Center, Iowa City, Iowa.
Correspondence to Allyn L. Mark, MD, Roy J. Carver Professor of Medicine, University of Iowa College of Medicine, 200 MAB, The University of Iowa, Iowa City, IA 52242. E-mail allyn-mark{at}uiowa.edu
AbstractObesity is associated with an increased risk of hypertension. In the past 5 years there have been dramatic advances into the genetic and neurobiological mechanisms of obesity with the discovery of leptin and novel neuropeptide pathways regulating appetite and metabolism. In this brief review, we argue that these mounting advances into the neurobiology of obesity have and will continue to provide new insights into the regulation of arterial pressure in obesity. We focus our comments on the sympathetic, vascular, and renal mechanisms of leptin and melanocortin receptor agonists and on the regulation of arterial pressure in rodent models of genetic obesity. We suggest 3 concepts. First, the effect of obesity on blood pressure may depend critically on the genetic-neurobiological mechanisms underlying the obesity. Second, obesity is not consistently associated with increased blood pressure, at least in rodent models. Third, the blood pressure response to obesity may be critically influenced by modifying alleles in the genetic background.
Key Words: leptin melanocortins sympathetic nervous system agouti rats, experimental obesity
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