Linked Life Data

15702350

Source:http://linkedlifedata.com/resource/pubmed/id/15702350

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-3-21
pubmed:abstractText
Delayed rectifier K(+) currents (I(K)) play a critical role in determining cardiac action potential duration (APD). Modulation of I(K) affects cardiac excitability critically. There are three components of cardiac delayed rectifier, and the slowly activating component (I(Ks)) is influenced strongly by a variety of stimuli. Plasma levels of noradrenaline and endothelin are elevated in heart failure, and arrhythmias are promoted by such humoral abnormalities through modulation of ion channels. It has been reported that protein kinase A (PKA) and protein kinase C (PKC) modulate I(Ks) from human minK in a complex manner. In the present study, we coexpressed human minK with the human beta(1)-adrenoceptor (hbeta(1)AR) and the endothelin receptor subtype A (hET(A)R) in Xenopus oocytes and investigated the effects of receptor activation on the currents (I(Ks)) flowing through the oocytes. ET-1 modulated I(Ks) biphasically: a transient increase followed by a decrease. The PKC inhibitor chelerythrine completely inhibited the effects of ET-1. Intracellular EGTA abolished the transient increase by ET-1 and partially inhibited the subsequent decrease in the currents. When I(Ks) was increased by 10(-6) M isoproterenol (ISO), ET-1 did not increase but rather decreased the current to an even greater extent than under control conditions. In addition, the effects of ISO on I(Ks) were suppressed by ET(A)R stimulation. These data indicate that I(Ks) can be regulated by cross-talk between the ET(A)R and beta(1)AR systems in addition to direct regulation by each receptor system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0028-1298
pubmed:author
pubmed:issnType
Print
pubmed:volume
371
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-40
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Cross-talk between beta(1)-adrenoceptors and ET(A) receptors in modulation of the slow component of delayed rectifier K(+) currents.
pubmed:affiliation
Department of Cardiovascular Pharmacology, Yamagata University School of Medicine, 2-2-2 Iida-nishi, Yamagata 990-9585, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't