Linked Life Data

7834843

Source:http://linkedlifedata.com/resource/pubmed/id/7834843

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-2-28
pubmed:abstractText
The whole-cell patch-clamp technique was used to characterize the effects of several tyrosine kinase inhibitors on the voltage-gated K+ current (IK) in rat and rabbit pulmonary artery cells. IK was blocked in a dose-dependent manner by genistein (20 to 100 mumol/L) and ST 638 (0.5 to 40 mumol/L) but not by the inactive genistein analogue diadzein (100 mumol/L). This inhibition was not significantly altered when ATP was excluded from the patch pipette or when it was replaced by the poor tyrosine kinase substrate ATP-gamma-S. The inhibition was also unaffected by inclusion of the tyrosine phosphatase inhibitor orthovanadate in either the bath (0.5 mmol/L) or pipette (0.2 mmol/L) solutions. In the rat, IK ordinarily inactivated negligibly over 300 ms. In the presence of 10 mumol/L ST 638, however, IK reached a peak approximately 5 ms after depolarization (to +60 mV) and then decayed markedly. In the rabbit, IK demonstrated a prominent rapidly decaying initial component that was only slightly inhibited by ST 638, which preferentially blocked the sustained current; genistein showed the opposite selectivity. These observations indicated that IK blockade by genistein and ST 638 was not mediated by an inhibition of tyrosine kinase activity and further suggested that in both types of cells genistein and ST 638 preferentially blocked rapidly and slowly inactivating components of IK, respectively.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
310-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Inhibition of vascular smooth muscle cell K+ currents by tyrosine kinase inhibitors genistein and ST 638.
pubmed:affiliation
Department of Pharmacology, United Medical School, Guy's Hospital, London, England.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't