The detection of a functional I(Kur) current in the canine ventricle challenges the assumption that I(Kur) is strictly atrium-specific, which has implications for the safety and targeting of IKur blockers in atrial tachyarrhythmia therapy.
The cardiac ultrarapid outward current I(Kur), encoded by KCNA5, is of special pharmacological interest, because it is considered to be atrium-specific. I(Kur) has therefore become a target in the therapy of atrial tachyarrhythmias. However, the concept of atrium specificity is only valid if a functional I(Kur) current is in fact absent from the ventricle. However, new work has detected a I(Kur)-like current in canine ventricular myocytes, sensitive to 4-aminopyridine and suppressed by the I(Kur) blocker DPO-1, findings that support the existence of a functional ventricular I(Kur). These indications are, however, indirect and more effort is needed to clarify unequivocally the putative role of an expectedly small I(Kur) component in the ventricle.
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Erich Wettwer (2007) studied this question.
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