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

• Autor(a) principal: Cavadas, Cláudia
• Data de Publicação: 2007
• Outros Autores: Waeber, Bernard, Pedrazzini, Thierry, Grand, Daniela, Aubert, Jean-François, Buclin, Thierry, Grouzmann, Eric
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10316/5863; https://doi.org/10.1016/j.peptides.2006.11.022
• topic: Neuropeptide Y; Y1 knock-out mice; Plasma catecholamine; Cold pressor test; Heart rate; Arterial blood pressure; Baroreflex

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 Y1 knock-out mice (Y1-/-) than in wild-type mice (Y1+/+). The aim of this work was to study the hemodynamic response of Y1-/- mice to an acute stimulation of the sympathetic nervous system (cold pressor test, CPT). Plasma catecholamine concentrations were higher in Y1-/- 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 15 min 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 Y1-/- and Y1+/+ mice. In conclusion, mice lacking the Y1 receptor can maintain normal hemodynamic response to an acute activation of the sympathetic system, albeit at the expense of increased catecholamine discharge.