Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-4-28
pubmed:abstractText
Extracellular ATP concentration can rise because of its release by nerve terminals and by damaged cells during ischemia. After the activation of P2-purinergic receptors, ATP induces a positive inotropic effect and increases the L-type Ca2+ current via activation of a Gs protein but without cAMP production. In addition, ATP shifts the voltage characteristics of Ca2+ current toward hyperpolarized potentials. If ATP produced similar effects on the Na+ current (INa), this compound should also affect cardiac excitability and conduction. Using the whole-cell patch-clamp to record INa in rat ventricular cells, we show that extracellular application of ATP induced hyperpolarizing shifts in the current-voltage relation and the availability of INa. The ED50 for the shifts in both conductance and availability was obtained with 0.7 mumol/L ATP. Maximal shifts in conductance and availability were respectively 9.7 +/- 0.6 and 10.6 +/- 0.7 mV. The leftward shift of the availability curve is responsible for the decrease of INa amplitude at less polarized holding potentials. These effects were not cholera toxin sensitive and thus cannot be attributed to activation of the Gs protein. At 100 mumol/L, ATP gamma S and alpha,beta-methylene ATP could induce shift, whereas UTP and beta,gamma-methylene ATP as well as ADP and adenosine were without effect. Thus, depending on the resting membrane potential, ATP should either enhance excitability or favor slow conduction and weaken cardiac electrical homogeneity and consequently favor arrhythmia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
710-7
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Effect of extracellular ATP on the Na+ current in rat ventricular myocytes.
pubmed:affiliation
Laboratoire de Physiologie Cellulaire Cardiaque, INSERM U-241, Université Paris-Sud, Orsay, France.
pubmed:publicationType
Journal Article