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NPY Y1 receptor is not involved in the hemodynamic response to an acute cold pressor test in mice.

Authors
  • Cavadas, Cláudia
  • Waeber, Bernard
  • Pedrazzini, Thierry
  • Grand, Daniela
  • Aubert, Jean-François
  • Buclin, Thierry
  • Grouzmann, Eric
Type
Published Article
Journal
Peptides
Publisher
Elsevier
Publication Date
Feb 01, 2007
Volume
28
Issue
2
Pages
315–319
Identifiers
PMID: 17222943
Source
Medline
License
Unknown

Abstract

The vasoconstrictor neuropeptide Y (NPY) has been shown to down-regulate tyrosine hydroxylase expression in cultured adrenal chromaffin cells, which probably accounts for the higher plasma resting norepinephrine (NE) and epinephrine (E) concentrations observed in Y(1) knock-out mice (Y(1)-/-) than in wild-type mice (Y(1)+/+). The aim of this work was to study the hemodynamic response of Y(1)-/- mice to an acute stimulation of the sympathetic nervous system (cold pressor test, CPT). Plasma catecholamine concentrations were higher in Y(1)-/- mice than in wild-type animals at the end of the CPT. The CPT-induced increase in mean arterial blood pressure (MAP) and heart rate (HR) was similar in both genotypes. Independently of the genotype, females had significantly slower HR than males throughout the 15min duration of the CPT. There was no difference in the sensitivity of the baroreceptor reflex, as reflected by the change in HR divided by the concurrent change in MBP between Y(1)-/- and Y(1)+/+ mice. In conclusion, mice lacking the Y(1) receptor can maintain normal hemodynamic response to an acute activation of the sympathetic system, albeit at the expense of increased catecholamine discharge.

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