• 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