This report describes a hitherto unreported anionic background current from human atrial cardiomyocytes. Under whole-cell patch-clamp with anion-selective conditions, an outwardly rectifying anion current (IANION) was observed, which was larger with iodide than nitrate, and with nitrate than chloride as charge carrier. In contrast with a previously identified background anionic current from small mammal cardiomyocytes, IANION was not augmented by the pyrethroid tefluthrin (10 μM); neither was it inhibited by hyperosmolar external solution nor by DIDS (200 μM); thus IANION was not due to basal activity of volume-sensitive anion channels. IANION was partially inhibited by the Cl− channel blockers NPPB (50 μM) and Gly H-101 (30 μM). Incorporation of IANION into a human atrial action potential (AP) simulation led to depression of the AP plateau, accompanied by alterations to plateau inward calcium current, and to AP shortening at 50% but not 90% of complete repolarization, demonstrating that IANION can influence the human atrial AP profile.

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