title: Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein-vasopressin fusion gene.
abstract: 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 1.0M NaCl, 1 microl/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 V1 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 V1 receptor in the PVN magnocellular neurons.
authors.affiliation: Department of Physiology, Miyazaki Medical College, University of Miyazaki, 5200 Kihara, Kiyotake-cho, Miyazaki-gun, Miyazaki 889 1692, Japan.
authors.forename: Chun-Ping
authors.initials: CP
authors.lastname: Chu
authors.forename: Kazuo
authors.initials: K
authors.lastname: Kato
authors.forename: Qing-Hua
authors.initials: QH
authors.lastname: Jin
authors.forename: De-Lai
authors.initials: DL
authors.lastname: Qiu
authors.forename: Nan-Shou
authors.initials: NS
authors.lastname: Yu
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Oiso
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kannan
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D065092:Antidiuretic Hormone Receptor Antagonists; D001120:Arginine / Q000235:genetics; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002319:Cardiovascular System / Q000187:drug effects*; D003243:Consciousness; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D008297:Male; D008668:Metallothionein / Q000235:genetics*; D016761:Oncogene Proteins v-fos / Q000096:biosynthesis* / Q000187:drug effects; D010880:Piperidines / Q000494:pharmacology; D015363:Quinolones / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017483:Receptors, Vasopressin / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000235:genetics; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage*; D012965:Sodium Chloride / Q000008:administration & dosage; D014667:Vasopressins / Q000235:genetics*
chemical_list: D065092:Antidiuretic Hormone Receptor Antagonists; D016761:Oncogene Proteins v-fos; D010880:Piperidines; D015363:Quinolones; D017483:Receptors, Vasopressin; D011993:Recombinant Fusion Proteins; D012462:Saline Solution, Hypertonic; D014667:Vasopressins; C068644:OPC 21268; D012965:Sodium Chloride; D008668:Metallothionein; D001120:Arginine