4.3 Article

Brain vasopressin V1 receptors contribute to enhanced cardiovascular responses to acute stress in chronically stressed rats and rats with myocardial infarcton

出版社

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00543.2009

关键词

vasopressin 1 receptor antagonist; heart failure; tachycardia; depression

资金

  1. Ministery of Science and Education [2P05 182 29]
  2. Medical University of Warsaw [1MA/W2/2006-2008]

向作者/读者索取更多资源

Cudnoch-Jedrzejewska A, Szczepanska-Sadowska E, Dobruch J, Gomolka R, Puchalska L. Brain vasopressin V-1 receptors contribute to enhanced cardiovascular responses to acute stress in chronically stressed rats and rats with myocardial infarcton. Am J Physiol Regul Integr Comp Physiol 298: R672-R680, 2010. First published December 30, 2009; doi:10.1152/ajpregu.00543.2009.-The present study was designed to determine the role of central vasopressin 1 receptors (V1R) in the regulation of cardiovascular parameters in chronically stressed infarcted rats and sham-operated rats under resting conditions and during exposure to acute alarming stress. The experiments were performed on four groups of conscious sham-operated and four groups of infarcted rats subjected to intraventricular infusion of either vehicle or a V1R antagonist (V(1)RANT). Two groups of infarcted and two groups of sham-operated rats were subjected to mild chronic stressing. Mean arterial blood pressure (MABP) and heart rate (HR) were determined under resting conditions and after exposure to acute stress (air jet). During vehicle infusion, MABP and HR increases in response to acute stress in the infarcted rats not subjected to chronic stress, and in the infarcted and sham-operated chronically stressed rats, were significantly greater than in the sham-operated rats not exposed to chronic stress. However, MABP and HR responses to acute stress in the chronically stressed infarcted rats and chronically stressed sham-operated rats did not differ. V(1)RANT abolished differences in cardiovascular responses to acute stress between the experimental groups. Resting cardiovascular parameters were not affected by any of the experimental treatments. It is concluded that chronic stressing enhances the pressor and tachycardic responses to acute stress in the sham-operated rats but does not further intensify these responses in infarcted rats. The results provide evidence that central V(1)Rs are involved in potentiation of cardiovascular responses to acute stress in chronically stressed rats, infarcted rats, and chronically stressed infarcted rats.

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