Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1991-4-22
pubmed:abstractText
The current study was designed to analyse the mechanisms which are impaired in the vascular hyporeactivity to contractile agents induced by E. coli lipopolysaccharide endotoxin (LPS). Endothelium-denuded aortic rings were prepared from thoracic aorta removed from control and LPS-pretreated rats (20 mg/kg i.p., 4 h before the experiment). In order to determine whether LPS treatment altered the contractile components that depend on intracellular calcium release and extracellular calcium entry to the same extent, rings were contracted under various experimental conditions. The responses elicited by indanidine, phenylephrine (without and with nitrendipine 1 microM), (-) Bay K 8644, (+) S 202-791 and the calcium ionophore calimycin in the presence of 1.25 mM external CaCl2 were all impaired by LPS pretreatment (maximal contractions 19, 63, 44, 28, 22 and 22% of controls, respectively). Concentration-effect curves for CaCl2 made in depolarizing medium (KCl 40 and 100 mM) and in the presence of calimycin (3 microM) were shifted to the right in rings from LPS-pretreated rats. However, the LPS-induced depression of contraction was overcome by the addition of CaCl2 (up to 30 mM). Additionally, in the absence of external CaCl2, the contraction induced by caffeine (50 mM) was not significantly altered by LPS treatment. It is concluded that LPS treatment does not reduce the ability of aortic smooth muscle cells to contract. The results suggest that LPS treatment impairs mechanisms involved in calcium handling within smooth muscle cells after stimulation of calcium entry through different pathways and activation of intracellular calcium release by alpha 1-adrenoceptor agonists.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/3-Pyridinecarboxylic acid..., http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Caffeine, http://linkedlifedata.com/resource/pubmed/chemical/Calcimycin, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Clonidine, http://linkedlifedata.com/resource/pubmed/chemical/Endotoxins, http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate, http://linkedlifedata.com/resource/pubmed/chemical/Nitrendipine, http://linkedlifedata.com/resource/pubmed/chemical/Phenylephrine, http://linkedlifedata.com/resource/pubmed/chemical/Potassium Chloride, http://linkedlifedata.com/resource/pubmed/chemical/indanidine
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
190
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
185-92
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1706272-3-Pyridinecarboxylic acid..., pubmed-meshheading:1706272-Adrenergic alpha-Agonists, pubmed-meshheading:1706272-Animals, pubmed-meshheading:1706272-Aorta, Thoracic, pubmed-meshheading:1706272-Caffeine, pubmed-meshheading:1706272-Calcimycin, pubmed-meshheading:1706272-Calcium, pubmed-meshheading:1706272-Clonidine, pubmed-meshheading:1706272-Endothelium, Vascular, pubmed-meshheading:1706272-Endotoxins, pubmed-meshheading:1706272-Inositol 1,4,5-Trisphosphate, pubmed-meshheading:1706272-Male, pubmed-meshheading:1706272-Muscle, Smooth, Vascular, pubmed-meshheading:1706272-Muscle Contraction, pubmed-meshheading:1706272-Nitrendipine, pubmed-meshheading:1706272-Phenylephrine, pubmed-meshheading:1706272-Potassium Chloride, pubmed-meshheading:1706272-Rats, pubmed-meshheading:1706272-Rats, Inbred Strains, pubmed-meshheading:1706272-Sarcoplasmic Reticulum
pubmed:year
1990
pubmed:articleTitle
Endotoxin-induced impairment of vascular smooth muscle contractions elicited by different mechanisms.
pubmed:affiliation
Laboratoire de Pharmacologie Cellulaire et Moléculaire (CNRS URA 0600), Université Louis Pasteur de Strasbourg, Illkirch, France.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't