Over-expression of V1A receptors in PVN modulates autonomic cardiovascular control

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• 作者：Maja Lozić^a ; Tatjana Tasić^a ; Andrew Martin^b ; Michael Greenwood^b ; Olivera &Scaron ; arenac^a ; ^b ; Charles Hindmarch^b ; ^d ; Julian F. Paton^c ; David Murphy^b ; ^d ; Nina Japundžić-Žigon^a ; ^{nzigon@med.bg.ac.rs} ; ^{nina.japundzic@gmail.com}
• 关键词：BRS ; baroreflex sensitivity ; VLF ; very low frequency short-term variability ; LF ; low frequency short-term variability ; HF ; high frequency short-term variability ; VP ; vasopressin ; OT ; oxytocin ; OTR ; oxytocin receptor ; V1aR ; vasopressin V1a receptor ; V1bR ; vasopressin V1b receptor ; V2R ; vasopressin V2 receptor ; V1aRX ; vasopressin V1a receptor antagonist ; PVN ; paraventricular nucleus ; NTS ; nucleus of the solitary tract ; RVLM ; rostroventrolateral medulla ; IML ; intermediolateral column of the spinal
• 刊名：Pharmacological Research
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：114
• 期：Complete
• 页码：185-195
• 全文大小：2106 K
• 卷排序：114

文摘

The hypothalamic paraventricular nucleus (PVN) is a key integrative site for the neuroendocrine control of the circulation and of the stress response. It is also a major source of the neuropeptide hormone vasopressin (VP), and co-expresses V1a receptors (V1aR). We thus sought to investigate the role of V1aR in PVN in cardiovascular control in response to stress. Experiments were performed in male Wistar rats equipped with radiotelemetric device. The right PVN was transfected with adenoviral vectors (Ads) engineered to over-express V1aR along with an enhanced green fluorescent protein (eGFP) tag. Control groups were PVN transfected with Ads expressing eGFP alone, or wild-type rats (Wt). Rats were recorded with and without selective blockade of V1aR (V1aRX) in PVN under both baseline and stressed conditions. Blood pressure (BP), heart rate (HR), their short-term variabilities, and baroreflex sensitivity (BRS) were evaluated using spectral analysis and the sequence method, respectively. Under baseline physiological conditions,V1aR rats exhibited reduced BRS and a marked increase of BP and HR variability during exposure to stress. These effects were all prevented by V1aRX pretreatment. In Wt rats, V1aRX did not modify cardiovascular parameters under baseline conditions, and prevented BP variability increase by stress. However, V1aRX pretreatment did not modify baroreflex desensitization by stress in either rat strain. It follows that increased expression of V1aR in PVN influences autonomic cardiovascular regulation and demarcates vulnerability to stress. We thus suggest a possible role of hypothalamic V1aR in cardiovascular pathology.