Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein-vasopressin fusion gene

Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein-vasopressin fusion gene
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DOI:
10.1016/j.neures.2005.06.011
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发表时间:
2005-10-01
影响因子:
2.9
通讯作者:
Kannan, H
Kannan, H
中科院分区:
医学4区
文献类型:
--
作者:
Chu, CP;Kato, K;Kannan, H

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本研究观察了大鼠侧脑室注射(i. c. v.)在清醒的精氨酸加压素(AVP)过表达转基因(Tg)大鼠和对照大鼠中施用高渗盐水(HS)。中央HS(0.3,0.67或1.0 M NaCl,1 μ l/min,持续20 min)显著增加平均动脉血压(MABP)和下丘脑室旁核(PVN)和视上核(SON)、最后区(AP)、正中视前核(MnPO)、和终板血管器(OVLT)。Tg大鼠MABP和FLI的变化明显大于对照组。静脉注射AVP V-1受体拮抗剂OPC-21268预处理可阻断MABP的升高,并显着降低0.3 M HS诱导的PVN(后部大细胞(pm)成分)中Fos的表达。本研究表明,增加的反应性静脉注射给药HS AVP Tg大鼠,这表明加压素驱动和中央心血管反应之间的关系,通过,至少部分地,V-1受体的PVN magnocellular神经元。(c)2005年Elsevier爱尔兰有限公司和日本神经科学学会。All rights reserved.
The present study is an investigation of the responses of the cardiovascular system and Fos expression to intracerebroventricular (i.c.v.) administration of hypertonic saline (HS) in conscious arginine vasopressin (AVP)-overexpressing transgenic (Tg) and control rats. Central HS (0.3, 0.67, or 1.0 M NaCl, 1 mu l/min for 20 min) significantly increased the mean arterial blood pressure (MABP) and Fos-like immunoreactivity (FLI) in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus, the area postrema (AP), the median preoptic nucleus (MnPO), and the organum vasculosum laminae terminalis (OVLT) in both Tg and control rats. The changes in MABP and FLI were significantly larger in Tg rats than in control rats. i.c.v. pretreatment with the AVP V-1 receptor antagonist, OPC-21268, blocked the increase in MABP and significantly decreased the Fos expression in the PVN (posterior magnocellular (pm) component) induced by 0.3 M HS in the Tg rats. The present study demonstrates an increased responsiveness to i.c.v. administration of HS in AVP Tg rats, suggesting the relationship between the vasopressinergic drive and central cardiovascular response via, at least in part, the V-1 receptor in the PVN magnocellular neurons. (c) 2005 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.