Document Detail


The roles of V1a vasopressin receptors in blood pressure homeostasis: a review of studies on V1a receptor knockout mice.
MedLine Citation:
PMID:  22038263     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
A prompt rise in blood pressure occurs when arginine-vasopressin is administered in quantities adequate to activate vascular V1a subtype vasopressin receptors. However, it has been controversial whether the endogenous vasopressin-V1a system contributes to the maintenance of basal blood pressure during normal development and aging. Mutant mice lacking the V1a receptor gene (V1a(-/-)) show significantly lower blood pressure compared to control mice, without a notable change in heart rate. In V1a(-/-) mice, arterial baroreceptor reflexes were attenuated due to malfunctioning baroreflex center, and the mice's circulating blood volume was significantly reduced. In line with this reduction in circulating blood volume, adrenocortical hormone release was attenuated; plasma aldosterone levels were reduced and adrenocorticotropic hormone-stimulated corticosteroid release was attenuated. In addition, V1a receptor expression was detected in macula densa cells of the kidneys, which may have facilitated renin production from the juxtaglomerular cells. Deletion of the V1a receptor appears to impact the renin-angiotensin-aldosterone system. Studies on V1a(-/-) mice revealed that non-vascular V1a receptors in the central nervous system and peripheral tissues play critical roles in the maintenance of blood pressure homeostasis.
Authors:
Yoko Fujiwara; Akito Tanoue; Gozoh Tsujimoto; Taka-Aki Koshimizu
Related Documents :
7033283 - Hemodynamics in diabetic orthostatic hypotension.
6645873 - Fluid shifts in vascular and extravascular spaces during and after simulated weightless...
6464053 - Non-invasive diagnosis of mild to severe stenosis of the internal carotid artery.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-11-1
Journal Detail:
Title:  Clinical and experimental nephrology     Volume:  -     ISSN:  1437-7799     ISO Abbreviation:  -     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-10-31     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9709923     Medline TA:  Clin Exp Nephrol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Division of Molecular Pharmacology, Department of Pharmacology, Jichi Medical University, 3311-1 Shimotsuke, Yakushiji, Tochigi, 329-0498, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Regulation and dysregulation of epithelial Na(+) channels.
Next Document:  Proteolytic activation of the epithelial sodium channel and therapeutic application of a serine prot...