Title of article
Hemodynamic consequences of neuropeptide Y-induced obesity
Author/Authors
Marcelo L. G. Correia، نويسنده , , Donald A. Morgan، نويسنده , , William I. Sivitz، نويسنده , , Allyn L. Mark، نويسنده , , William G. Haynes، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2002
Pages
6
From page
137
To page
142
Abstract
Background
Acute central nervous system administration of neuropeptide Y (NPY) elicits variable hemodynamic responses. Chronic intracerebroventricular (ICV) administration of NPY produces obesity in rats. Obesity has been shown to increase arterial pressure.
Methods
In this study we examined the chronic hemodynamic effects of NPY-induced obesity. Sprague-Dawley rats were implanted with radiotelemetry transmitters to continuously record heart rate and arterial pressure in the conscious state. Neuropeptide Y or vehicle was delivered into the third cerebral ventricle by osmotic minipumps over 2 weeks. Three groups were studied: vehicle, NPY-treated (free-fed), and NPY-treated (pair-fed to vehicle-treated rats).
Results
Neuropeptide Y increased food intake and body weight in free-fed animals, and substantially augmented visceral adiposity in both free- and pair-fed rats. Despite increased adiposity, chronic ICV administration of NPY in conscious unstressed rats did not increase arterial pressure. Neuropeptide Y decreased heart rate, suggesting a sympathoinhibitory effect.
Conclusions
Obesity induced by 2-week ICV administration of NPY does not increase arterial pressure, perhaps indicating inhibition of sympathetic outflow that may oppose the pressor effect of adiposity.
Keywords
Neuropeptide Y , obesity , Arterial pressure , Hypothalamus , sympathetic nervous system.
Journal title
American Journal of Hypertension
Serial Year
2002
Journal title
American Journal of Hypertension
Record number
648117
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