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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-1-9
pubmed:abstractText
The aim of this study was to determine the effects of vasopressin V1 receptor antagonism on regional hemodynamics in spontaneously hypertensive rats (SHR/Izm). Changes in blood flow in the superior mesenteric artery or terminal aorta were measured in rats with a chronically implanted electromagnetic flowmeter. The combination of a non-hypotensive hemorrhage (0.3 ml/100 g weight) and ganglionic blockade with hexamethonium bromide (C6; 25 mg/kg weight) had no effect on mesenteric resistance. On the other hand, subsequent intravenous administration of a peptide vasopressin V1 receptor antagonist (V1A; 10 microg/kg:[d(CH2)5(1)-O Methyl-Tyr(2)-Arg8]-vasopressin) significantly reduced mesenteric resistance in SHR/Izm but had no effect on hindquarter resistance. Furthermore, the infusion of C6 (after pretreatment with hemorrhage plus V1A) induced a marked reduction of blood pressure and a significant decrease in superior mesenteric resistance only in SHR/Izm. Thus, we showed an altered reactivity to V1A in the superior mesenteric and/or hindquarter vascular regions of SHR/Izm, suggesting that maintenance of elevated resistance in the mesenteric vascular bed mainly relates to a potential vasopressin-mediated vasoconstriction and that a new sympathetic vasoconstrictor tone is generated within the superior mesenteric vascular bed to compensate for hypotensive intervention (minor hemorrhage plus V1A) in conscious SHR/Izm.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0018-2052
pubmed:author
pubmed:issnType
Print
pubmed:volume
54
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
93-9
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
V1 receptor activation induced by hemorrhage and sympathoinhibition in the mesentery and hindquarters of spontaneously hypertensive rats.
pubmed:affiliation
Department of Neurophysiology, Graduate School of Biomedical Sciences, Hiroshima University, Minami-ku, Hiroshima 734-8551, Japan.
pubmed:publicationType
Journal Article