Linked Life Data

16395254

Source:http://linkedlifedata.com/resource/pubmed/id/16395254

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-2-9
pubmed:abstractText
Lead exposure induces dysfunction of the cyclic guanosine monophosphate-dependent vasodilator system through downregulation of soluble guanylate cyclase (sGC) expression. The endothelium not only releases vasodilators but also vasoconstrictors such as endothelin-1 (ET-1). Our aim was to explore the role of the vascular endothelium and ET-1 as possible mediators of lead-induced downregulation of sGC. Isolated aortic segments from Wistar Kyoto rats were incubated in the presence or absence of lead (1 parts per million) for 24 h. Endothelium was mechanically removed in some of the aorta segments. As reported previously, lead exposure induced downregulation of sGC protein expression in the intact aortic segments. However, lead exposure failed to significantly modify sGC-beta1 subunit expression in the endothelium-denuded aortic segments. Incubation with a selective ETA-type receptor inhibitor, BQ-123 (10(-6) mol/l), restored sGC protein expression in lead-exposed intact aortic segments. As it has also been previously observed, incubation in lead-containing medium resulted in the upregulation of cyclooxygenase-2 (COX-2) in the intact aortic segments. Denudation of endothelium partially abrogated this effect of lead. Incubation with BQ-123 prevented the lead-induced upregulation COX-2 in the intact aortic segments. However, neither ET-1 content nor ETA-type receptor expression were modified by lead exposure of the aortic segments. As conclusion, the endothelium through the activation of ETA-type receptors mediates the downregulation of sGC expression by lead in the vascular wall.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
685-90
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16395254-Animals, pubmed-meshheading:16395254-Antihypertensive Agents, pubmed-meshheading:16395254-Aorta, pubmed-meshheading:16395254-Blotting, Western, pubmed-meshheading:16395254-Cyclooxygenase 2, pubmed-meshheading:16395254-Down-Regulation, pubmed-meshheading:16395254-Endothelin-1, pubmed-meshheading:16395254-Endothelium, Vascular, pubmed-meshheading:16395254-Guanylate Cyclase, pubmed-meshheading:16395254-Lead, pubmed-meshheading:16395254-Male, pubmed-meshheading:16395254-Membrane Proteins, pubmed-meshheading:16395254-Muscle, Smooth, Vascular, pubmed-meshheading:16395254-Myocytes, Smooth Muscle, pubmed-meshheading:16395254-Peptides, Cyclic, pubmed-meshheading:16395254-Rats, pubmed-meshheading:16395254-Rats, Inbred WKY, pubmed-meshheading:16395254-Receptor, Endothelin A, pubmed-meshheading:16395254-Vasodilation
pubmed:year
2006
pubmed:articleTitle
Involvement of endothelium and endothelin-1 in lead-induced smooth muscle cell dysfunction in rats.
pubmed:affiliation
Cardiovascular Research Unit, Hospital Clínico San Carlos, Madrid, Spain, and Department of Medicine, University of California, Irvine, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't