Linked Life Data

17872465

Source:http://linkedlifedata.com/resource/pubmed/id/17872465

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2007-11-9
pubmed:abstractText
Carotid body chemoreceptors sense hypoxemia, hypercapnia, and acidosis and play an important role in cardiorespiratory regulation. The molecular mechanism of pH sensing by chemoreceptors is not clear, although it has been proposed to be mediated by a drop in intracellular pH of carotid body glomus cells, which inhibits a K+ current. Recently, pH-sensitive ion channels have been described in glomus cells that respond directly to extracellular acidosis. In this study, we investigated the possible molecular mechanisms of carotid body pH sensing by recording the responses of glomus cells isolated from rat carotid body to rapid changes in extracellular pH using the whole-cell patch-clamping technique. Extracellular acidosis evoked transient inward current in glomus cells that was inhibited by the acid-sensing ion channel (ASIC) blocker amiloride, absent in Na+-free bathing solution, and enhanced by either Ca2+-free buffer or addition of lactate. In addition, ASIC1 and ASIC3 were shown to be expressed in rat carotid body by quantitative PCR and immunohistochemistry. In the current-clamp mode, extracellular acidosis evoked both a transient and sustained depolarizations. The initial transient component of depolarization was blocked by amiloride, whereas the sustained component was eliminated by removal of K+ from the pipette solution and partially blocked by the TASK (tandem-p-domain, acid-sensitive K+ channel) blockers anandamide and quinidine. The results provide the first evidence that ASICs may contribute to chemotransduction of low pH by carotid body chemoreceptors and that extracellular acidosis directly activates carotid body chemoreceptors through both ASIC and TASK channels.
pubmed:grant
pubmed:commentsCorrections
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
9
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1009-19
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17872465-Acidosis, pubmed-meshheading:17872465-Acids, pubmed-meshheading:17872465-Animals, pubmed-meshheading:17872465-Calcium, pubmed-meshheading:17872465-Carotid Body, pubmed-meshheading:17872465-Chemoreceptor Cells, pubmed-meshheading:17872465-Extracellular Space, pubmed-meshheading:17872465-Hydrogen-Ion Concentration, pubmed-meshheading:17872465-Ion Channel Gating, pubmed-meshheading:17872465-Membrane Potentials, pubmed-meshheading:17872465-Membrane Proteins, pubmed-meshheading:17872465-Nerve Tissue Proteins, pubmed-meshheading:17872465-Patch-Clamp Techniques, pubmed-meshheading:17872465-Potassium, pubmed-meshheading:17872465-RNA, Messenger, pubmed-meshheading:17872465-Rats, pubmed-meshheading:17872465-Sodium, pubmed-meshheading:17872465-Sodium Channels, pubmed-meshheading:17872465-Stimulation, Chemical
pubmed:year
2007
pubmed:articleTitle
Acid-sensing ion channels contribute to transduction of extracellular acidosis in rat carotid body glomus cells.
pubmed:affiliation
Cardiovascular Center and Department of Internal Medicine, University of Iowa, Iowa City, IA 52242, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural