Feedback remodeling of cardiac potassium current expression: a novel potential mechanism for control of repolarization reserve

Circulation
Ling XiaoStanley Nattel

Abstract

Inhibition of individual K(+) currents causes functionally based compensatory increases in other K(+) currents that minimize changes in action potential duration, a phenomenon known as repolarization reserve. The possibility that sustained K(+) channel inhibition may induce remodeling of ion current expression has not been tested. Accordingly, we assessed the effects of sustained inhibition of one K(+) current on various other cardiac ionic currents. Adult canine left ventricular cardiomyocytes were incubated in primary culture and paced at a physiological rate (1 Hz) for 24 hours in the presence or absence of the highly selective rapid delayed-rectifier K(+) current (I(Kr)) blocker dofetilide (5 nmol/L). Sustained dofetilide exposure led to shortened action potential duration and increased repolarization reserve (manifested as a reduced action potential duration-prolonging response to I(Kr) blockade). These repolarization changes were accompanied by increased slow delayed-rectifier (I(Ks)) density, whereas I(Kr), transient-outward (I(to)), inward-rectifier (I(K1)), L-type Ca(2+) (I(CaL)), and late Na(+) current remained unchanged. The mRNA expression corresponding to KvLQT1 and minK (real-time polymerase chain reaction) was un...Continue Reading

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