Linked Life Data

7545106

Source:http://linkedlifedata.com/resource/pubmed/id/7545106

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1995-10-12
pubmed:abstractText
The pharmacological properties of voltage-gated Ca current and glucose-dependent insulin secretion were determined using the HIT insulinoma line to understand the role of Ca channels in stimulus-secretion coupling. The L-type Ca channel antagonist nimodipine inhibited a maximum of 50-55% of the peak Ca current, suggesting that L- and non-L-type channels contribute to Ca current. The L-agonist BAY K 8644 increased Ca current by 155%, whereas the N-channel blocker omega-conotoxin MVIIA reversibly blocked 35% of the peak Ca current. Total block with nimodipine and MVIIA was additive. Conotoxin MVIIC did not affect HIT Ca current. Prolonged depolarizations elicited rapidly and slowly inactivating Ca currents. Nimodipine partially inhibited transient current, but fully inhibited slowly inactivating current, suggesting that the former is mediated by L- and N-channels, and the latter is mediated by L-channels. Like slowly inactivating Ca current, glucose-dependent insulin secretion was fully inhibited by nimodipine and insensitive to MVIIA. BAY K potentiated secretion and antagonized nimodipine block. These results suggest that persistent Ca current is mediated by L-channels and is strongly coupled to insulin secretion, whereas transient Ca current is mediated by L- and N-channels and is weakly coupled. Sustained Ca influx may be preferentially coupled because glucose persistently depolarizes HIT cells and inactivates more transient Ca channel pathways.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
136
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4589-601
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Contribution of L- and non-L-type calcium channels to voltage-gated calcium current and glucose-dependent insulin secretion in HIT-T15 cells.
pubmed:affiliation
Department of Pharmacology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.