Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1997-11-5
pubmed:abstractText
Platelet aggregation and adherence to the vessel lumina are common events in various physiological and pathological conditions. However, the mechanisms whereby aggregating platelets cause vasoconstriction remain unclear. We hypothesized that aggregating platelets may alter the Ca2+ sensitivity of the contractile apparatus in smooth muscle cells. We tested this hypothesis using rabbit common carotid arteries permeabilized with beta-escin. In these preparations, the receptor-effector coupling is functionally intact, while the intracellular ionic composition, in particular calcium concentration, may be clamped. Aggregating platelets in the presence of 100 microM GTP left-shifted the pCa-force curve. On average, the pD2 for calcium was 6.30 +/- 0.05 and 6.86 +/- 0.07 in the absence and presence of platelets, respectively (p < 0.01). This increase in calcium sensitivity was prevented by blockade of G-proteins with guanosine 5'-O-(2-thiodiphosphate). Platelets modulated calcium sensitivity at concentrations markedly lower than those that produce contractions of intact vessels. These data suggest that platelet activation in the vicinity of the vessel wall may sensitize the smooth muscle contractile apparatus to calcium via a G-protein-dependent mechanism. This phenomenon may enhance vessel responses to vasoactive substance that produce vessel contraction via elevation of intracellular calcium concentrations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0008-4212
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
849-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Mechanisms of platelet-induced angiospastic reactions: potentiation of calcium sensitivity.
pubmed:affiliation
Department of Physiology, Loma Linda University School of Medicine, CA 92350, USA.
pubmed:publicationType
Journal Article, In Vitro