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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-12-6
pubmed:abstractText
We hypothesize that cerebral ischemia leads to enhanced expression of endothelin (ET), 5-hydroxytryptamine (5-HT), and angiotensin II (ANG II) receptors in the vascular smooth muscle cells. Our aim is to correlate the upregulation of cerebrovascular receptors and the underlying molecular mechanisms with the reduction in regional and global cerebral blood flow (CBF) after subarachnoid hemorrhage (SAH). SAH was induced by injecting 250 microl blood into the prechiasmatic cistern in rats. The cerebral arteries were removed 0, 1, 3, 6, 12, 24, and 48 h after the SAH for functional and molecular studies. The contractile responses to ET-1, 5-carboxamidotryptamine (5-CT), and ANG II were investigated with myograph. The receptor mRNA and protein levels were analyzed by quantitative real-time PCR and immunohistochemistry, respectively. In addition, regional and global CBFs were measured by an autoradiographic method. As a result, SAH resulted in enhanced contractions to ET-1 and 5-CT. ANG II [via ANG II type 1 (AT(1)) receptors] induced increased contractile responses [in the presence of the ANG II type 2 (AT(2)) receptor antagonist PD-123319]. In parallel the ET(B), 5-HT(1B), and AT(1) receptor, mRNA and protein levels were elevated by time. The regional and global CBF showed a successive reduction with time after SAH. In conclusion, the results demonstrate for the first time that SAH induces the upregulation of ET(B), 5-HT(1B), and AT(1) receptors in a time-dependent manner both at functional, mRNA, and protein levels. These changes occur in parallel with a successive decrease in CBF. Thus there is a temporal correlation between the changes in receptor expression and CBF reduction, suggesting a linkage.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
293
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H3750-8
pubmed:meshHeading
pubmed-meshheading:17873013-Angiotensin II, pubmed-meshheading:17873013-Animals, pubmed-meshheading:17873013-Autoradiography, pubmed-meshheading:17873013-Cerebral Arteries, pubmed-meshheading:17873013-Cerebrovascular Circulation, pubmed-meshheading:17873013-Disease Models, Animal, pubmed-meshheading:17873013-Dose-Response Relationship, Drug, pubmed-meshheading:17873013-Endothelin-1, pubmed-meshheading:17873013-Immunohistochemistry, pubmed-meshheading:17873013-Male, pubmed-meshheading:17873013-Muscle, Smooth, Vascular, pubmed-meshheading:17873013-Polymerase Chain Reaction, pubmed-meshheading:17873013-RNA, Messenger, pubmed-meshheading:17873013-Rats, pubmed-meshheading:17873013-Rats, Sprague-Dawley, pubmed-meshheading:17873013-Receptor, Angiotensin, Type 1, pubmed-meshheading:17873013-Receptor, Endothelin B, pubmed-meshheading:17873013-Receptor, Serotonin, 5-HT1B, pubmed-meshheading:17873013-Serotonin, pubmed-meshheading:17873013-Subarachnoid Hemorrhage, pubmed-meshheading:17873013-Time Factors, pubmed-meshheading:17873013-Up-Regulation, pubmed-meshheading:17873013-Vasoconstriction, pubmed-meshheading:17873013-Vasoconstrictor Agents
pubmed:year
2007
pubmed:articleTitle
Cerebrovascular ETB, 5-HT1B, and AT1 receptor upregulation correlates with reduction in regional CBF after subarachnoid hemorrhage.
pubmed:affiliation
Department of Clinical Sciences, Division of Experimental Vascular Research, Lund University, 221 84 Lund, Sweden. saema.ansar@med.lu.se
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't