Linked Life Data

14962843

Source:http://linkedlifedata.com/resource/pubmed/id/14962843

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-5-18
pubmed:abstractText
Intracellular Ca2+ transients were identified in endothelial cells (ECs) in intact blood-perfused arterioles. ECs in cremaster muscle arterioles (diameter approximately 45 microm) in anesthetized mice were loaded with the Ca2+ indicator fluo 4-AM by intraluminal perfusion, after which blood flow was reestablished. Confocal microscopy was used to visualize Ca2+ as a function of fluo-4 intensity in real time. Separate sets of experiments were performed under the following conditions: control, ischemia, during inhibition of P(2x) or P(1) purinoreceptors, and with the application of exogenous adenosine. In controls, spontaneous EC Ca2+ transients displayed a wide range of activity frequency (1-32 events/min) and about one-third of these transient events were synchronized between adjacent ECs. The increase in Ca2+ remained localized and did not spread to encompass the entire cell body. Ca2+ transient activity decreased significantly with ischemia (from 9.9 +/- 0.6 to 3.1 +/- 0.3 events/min, n = 135) but was unaffected by P(2x) or P(1) receptor inhibition. Exogenous adenosine significantly increased the frequency of Ca2+ transients (to 12.8 +/- 0.9 events/min) and increased synchronization so that 50% of all Ca2+ events were synchronized between ECs. This response to adenosine was not due to an increase in shear stress. These data indicate that localized Ca2+ transients are sensitive to flow conditions and, separately, to metabolically active pathways (exogenous adenosine), although the basal activity occurs independently of P(2x) or P(1) receptors. These transients may represent a mechanism by which individual EC responses are integrated to result in coordinated arteriolar responses in situ.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
286
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2322-31
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Localized transient increases in endothelial cell Ca2+ in arterioles in situ: implications for coordination of vascular function.
pubmed:affiliation
Department of Biomedical Engineering, University of Rochester Medical Center, Rochester, NY 14642, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.