Received June 6, 2005
Revised July 25, 2005
Accepted after revision August 8, 2005
Role of leptin in obesity-related hypertension
William G. Haynes 1*
1 University of Iowa
* To whom correspondence should be addressed. E-mail: william-g-haynes{at}uiowa.edu.
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Abstract |
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Obesity in humans causes hypertension, myocardial
hypertrophy, 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
sympathoactivation. 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
sympathoexcitatory and pressor actions. This selective
leptin resistance of obesity, coupled with
hyperleptinemia, 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
pharmacologic treatments of obesity and obesity-related
hypertension.
Key Words:
Hypertension, Obesity
