Linked Life Data

8869566

Source:http://linkedlifedata.com/resource/pubmed/id/8869566

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-1-29
pubmed:abstractText
To test the hypothesis that Ca2+ is released from intracellular store in the carotid body glomus cells during hypoxia, we stimultaneously measured chemosensory discharge and tissue PO2 of perfused-superfused cat carotid body before and during flow interruption in the presence and absence of extracellular [Ca2+] with and without thapsigargin (1-10 microM). Ca(2+)-free solution increased the latency of sensory response, and decreased the rate of rise and peak activity but thapsigargin significantly influenced these responses, without affecting oxygen consumption. Since thapsigargin depletes the intracellular Ca2+ store, and since Ca2+ is needed for the sensory discharge, these results suggest that intracellular release and influx of Ca2+ occur during hypoxia.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
12
pubmed:volume
709
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
141-4
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Thapsigargin enhances carotid body chemosensory discharge in response to hypoxia in zero [Ca2+]e: evidence for intracellular Ca2+ release.
pubmed:affiliation
Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia 19104-6085, USA. LAHIRI@A1.MSCF.UPENN.EDU
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.