Linked Life Data

12679141

Source:http://linkedlifedata.com/resource/pubmed/id/12679141

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2003-4-7
pubmed:abstractText
The dihydropyridine cilnidipine has been reported to induce a fast decay of the L-type Ca(2+) current, an effect distinct from the modulation of voltage-dependent inactivation. We performed a whole-cell patch-clamp study using A7r5 cells to analyse the changes in current decay induced by two structurally related dihydropyridines after the amount of the beta-subunit mRNA has been decreased by the antisense oligonucleotide. The Ba(2+) current underwent a single exponential decay indicating voltage-dependent inactivation. The tau value was greater in the antisense group than in the sense and nonsense groups. Equipotent doses of cilnidipine and nimodipine decreased the tau value, while only cilnidipine created an additional component with a smaller tau value (tau(cil): 35 ms) that showed voltage-independence. Treatment with antisense failed to alter this component (tau(cil): 38 ms). These results suggest that cilnidipine specifically exerts a second type of blocking action on L-type Ca(2+) channels that is not dependent on the beta-subunit.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
466
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-62
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Characterization of Ca2+ current inhibition by cilnidipine using a beta-subunit antisense oligonucleotide.
pubmed:affiliation
Department of Oral and Maxillofacial Surgery, Fukuoka Dental College, 2-15-1 Tamura, Sawara-ku, 814-0193, Fukuoka, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't