Linked Life Data

2224527

Source:http://linkedlifedata.com/resource/pubmed/id/2224527

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-12-7
pubmed:abstractText
Whole cell patch clamp recordings were made from type I cells of the neonatal rat carotid body, isolated and maintained in primary culture for up to 48 h. Depolarizing voltage steps applied from a holding potential of -70 mV evoked outward currents positive to approximately -30 mV. Currents were strongly blocked by extracellular tetraethylammonium (25 mM), and were therefore attributed to activation of voltage-dependent K+ channels. Currents were also suppressed by 4-aminopyridine, removal of extracellular Ca2+, and replacement of extracellular Ca2+ with Ba2+. These results suggest there are Ca2(+)-dependent and Ca2(+)-independent components of the K+ currents. No evidence was found to suggest that ATP-sensitive K+ channels were present. The effects of 3 chemoexcitatory agents (NaCN, almitrine and reduced extracellular pH) on K+ currents in isolated type I cells were investigated. All three agents suppressed K+ currents to similar degrees. The effects of lowered pH and NaCN were reversible, and NaCN-induced reductions occurred regardless of the presence of intracellular ATP. The effect of almitrine was irreversible for up to 30 min of recording. It is concluded that the reduction of K+ currents by chemoexcitants may play a role in the mechanism of chemotransduction in the carotid body.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
522
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
259-66
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Potassium currents recorded in type I carotid body cells from the neonatal rat and their modulation by chemoexcitatory agents.
pubmed:affiliation
University Laboratory of Physiology, Oxford, U.K.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't