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KCI등재 학술저널

Effect of Prostaglandins D<SUB>2</SUB>, E<SUB>2</SUB> and I<SUB>2</SUB> on the Regulation of K<SUB>ATP</SUB> Channel Activity in Rat Cardiac Myocytes

Effect of Prostaglandins D<SUB>2</SUB>, E<SUB>2</SUB> and I<SUB>2</SUB> on the Regulation of K<SUB>ATP</SUB> Channel Activity in Rat Cardiac Myocytes

<P> Contribution of prostaglandins D<SUB>2</SUB>, E<SUB>2</SUB> and I<SUB>2</SUB> (PGD<SUB>2, </SUB>PGE<SUB>2 </SUB>and PGI<SUB>2</SUB>) on the regulation of ATP-sensitive K<SUP>&#8290;</SUP> channel (K<SUB>ATP </SUB>channel) was investigated in isolated single rat ventricular cardiac myocytes using the patch clamp technique. PGD<SUB>2</SUB>, PGE<SUB>2</SUB> and PGI<SUB>2</SUB> did not affect K<SUB>ATP</SUB> channel activity in the inside-out patch, but increased channel activity in a dose-dependent manner when the channel activities were attenuated by the administration of 100 μM ATP to the internal solution in the inside-out patch. Channel activations by the prostaglandins were abolished by 50 μM glibenclamide, a K<SUB>ATP</SUB> channel blocker. Dose-response curves of relative channel activity against the ATP concentrations of internal solution in the inside-out patch were shifted to the right in the presence of those three prostaglandins. The rank order of the channel stimulatory potencies (as IC<SUB>50</SUB> for ATP) calculated from the dose-response curves were PGI<SUB>2</SUB> > PGD<SUB>2</SUB> > PGE<SUB>2</SUB>. Conductance of the channel was not changed by those three prostaglandins. In conclusion, we suggest that prostaglandins D<SUB>2</SUB>, E<SUB>2</SUB> and I<SUB>2</SUB> are involved in the regulation of K<SUB>ATP </SUB>channel activity in certain circumstances, and that those three prostaglandins may cause myocardial relaxation by opening K<SUB>ATP</SUB> channels, thus protecting the heart from ischema.

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