Linked Life Data

11090551

Source:http://linkedlifedata.com/resource/pubmed/id/11090551

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2000-12-1
pubmed:abstractText
Cell-cell communication in the arteriolar wall was examined using the Ca(2+)-sensitive indicator fura-2 and the Ca(2+) buffer BAPTA as means of measuring and buffering cellular Ca(2+). The experiments focused on the role of endothelial cell [Ca(2+)](i) in modulating phenylephrine (PE)-induced contractions in in vitro arterioles of the hamster cremaster. Fura-2-AM and BAPTA-AM were applied intraluminally to accomplish endothelium-specific loading. PE was applied to short segments of arterioles using pressure-pulse ejection from a micropipette. Under control conditions at the site of stimulation, PE elicited a strong vasoconstriction preceded by an increase in endothelial cell [Ca(2+)](i). A very small biphasic conducted response was observed at sites upstream from the stimulation site. BAPTA sharply reduced the measured Ca(2+) response in the endothelium. This was associated with an enhanced local contractile response. In addition, the biphasic conducted response was converted into a strong conducted vasoconstriction. PE caused an initial rise in smooth muscle [Ca(2+)](i) at the stimulated site, which was followed by a rapid decrease below baseline. Endothelial cell loading of BAPTA had minimal effect on the initial [Ca(2+)](i) peak but eliminated the secondary decrease in smooth muscle [Ca(2+)](i). Intraluminal application of charybdotoxin plus apamin mimicked the change in vasomotor state induced by BAPTA. These data lead us to hypothesize that, after smooth muscle stimulation, intercellular Ca(2+) signaling between smooth muscle and endothelium causes a secondary rise in endothelial cell Ca(2+), which triggers a hyperpolarizing event and initiates a conducted vasodilation. We conclude that smooth muscle and endothelium operate as a functional unit in these vessels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
24
pubmed:volume
87
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1048-54
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11090551-Animals, pubmed-meshheading:11090551-Arterioles, pubmed-meshheading:11090551-Calcium, pubmed-meshheading:11090551-Calcium Signaling, pubmed-meshheading:11090551-Cricetinae, pubmed-meshheading:11090551-Egtazic Acid, pubmed-meshheading:11090551-Endothelium, Vascular, pubmed-meshheading:11090551-Fluorescent Dyes, pubmed-meshheading:11090551-Fura-2, pubmed-meshheading:11090551-Gap Junctions, pubmed-meshheading:11090551-Intracellular Fluid, pubmed-meshheading:11090551-Male, pubmed-meshheading:11090551-Mesocricetus, pubmed-meshheading:11090551-Muscle, Skeletal, pubmed-meshheading:11090551-Muscle, Smooth, Vascular, pubmed-meshheading:11090551-Phenylephrine, pubmed-meshheading:11090551-Potassium Channel Blockers, pubmed-meshheading:11090551-Potassium Channels, pubmed-meshheading:11090551-Vascular Resistance, pubmed-meshheading:11090551-Vasoconstrictor Agents
pubmed:year
2000
pubmed:articleTitle
Integrated Ca(2+) signaling between smooth muscle and endothelium of resistance vessels.
pubmed:affiliation
First Department of Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.