Journal
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
Volume 22, Issue 2, Pages 135-140Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MNH.0b013e32835d0c05
Keywords
appetite; leptin; MC4R; melanocortin system; visceral fat
Categories
Funding
- National Heart, Lung and Blood Institute [P01 HL 51971]
- American Heart Association Scientist Development
Ask authors/readers for more resources
Purpose of review Obesity is a major worldwide health problem. Excess weight gain is the most significant preventable cause of increased blood pressure (BP) in patients with essential hypertension and increases the risk for cardiovascular and renal diseases. Our goal is to review the mechanisms that link obesity with hypertension, with special emphasis on the role of leptin and the brain melanocortin system in driving sympathetic activation in obesity. Recent findings Despite increased interest in obesity as a major risk for developing hypertension, the precise mechanisms linking excess weight gain with increases in BP are still elusive. Current evidence suggests that increased sympathetic nervous system (SNS) activity contributes to impaired renal-pressure natriuresis and sodium retention in obesity. Recent findings indicate that the adipocyte-derived hormone, leptin, activates brain centers that regulate SNS activity through a melanocortin-system-dependent pathway. The interaction of leptin and the brain melanocortin system represents an important area of research to further our understanding of the mechanisms leading to sympathetic activation in obesity. Summary Sympathetic overactivity is an important link between excess weight gain and increased BP. Hormones and cytokines secreted by the adipose tissue that interact with neural pathways (e.g. melanocortin system) appear to play a key role in contributing to sympathetic activation in obesity and represent potential new targets for therapies.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available