Blockade of central vasopressin receptors reduces the cardiovascular response to acute stress in freely moving rats

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• 作者：S. Stojid ; ić ; S. Milutinović ; -Smiljanić ; O. Š ; arenac ; S. Milosavljević ; J.F.R. Paton ; D. Murphy ; N. Japundž ; ić ; -d ; igon
• 关键词：V_1a ; V_1b ; V₂ ; Vasopressin ; Stress ; Blood pressure
• 刊名：Neuropharmacology
• 出版年：2008
• 期刊代码：33_00283908
• 类别：pha
• 出版时间：April 2008
• 卷：54
• 期：5
• 页码：824-836
• 文件大小：2654 K

摘要

To investigate the contribution of central vasopressin receptors to blood pressure (BP) and heart rate (HR) response to stress we injected non-peptide selective V_1a (SR49059), V_1b (SSR149415), V₂ (SR121463) receptor antagonists, diazepam or vehicle in the lateral cerebral ventricle of conscious freely moving rats stressed by blowing air on their heads for 2 min. Cardiovascular effects of stress were evaluated by analyzing maximum increase of BP and HR (MAX), latency of maximum response (LAT), integral under BP and HR curve (∫), duration of their recovery and spectral parameters of BP and HR indicative of increased sympathetic outflow (LF_BP and LF/HF_HR). Moreover, the increase of serum corticosterone was measured. Exposure to air-jet stress induced simultaneous increase in BP and HR followed by gradual decline during recovery while LF_BP oscillation remained increased as well as serum corticosterone level. Rats pre-treated with vasopressin receptor antagonists were not sedated while diazepam induced sedation that persisted during exposure to stress. V_1a, V_1b and V₂ receptor antagonists applied separately did not modify basal values of cardiovascular parameters but prevented the increase in ∫_BP. In addition, V_1b and V₂ receptor antagonists reduced BP_MAX whereas V_1a, V_1b antagonist and diazepam reduced HR_MAX induced by exposure to air-jet stress. All drugs shortened the recovery period, prevented the increase of LF_BP without affecting the increase in serum corticosterone levels. Results indicate that vasopressin receptors located within the central nervous system mediate, in part, the cardiovascular response to air-jet stress without affecting either the neuroendocrine component or inducing sedation. They support the view that the V_1b receptor antagonist may be of potential therapeutic value in reducing arterial pressure induced by stress-related disorders.