An outwardly rectifying anionic background current in atrial myocytes from the human heart.
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 (I(ANION)) 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, I(ANION) was not augmented by the pyrethroid tefluthrin (10 microM); neither was it inhibited by hyperosmolar external solution nor by DIDS (200 microM); thus I(ANION) was not due to basal activity of volume-sensitive anion channels. I(ANION) was partially inhibited by the Cl(-) channel blockers NPPB (50 microM) and Gly H-101 (30 microM). Incorporation of I(ANION) 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 I(ANION) can influence the human atrial AP profile.
Li
H
H
Department of Pharmacology, Bristol Heart Institute, School of Medical Sciences, The University of Bristol, University Walk, Bristol BS8 1TD, UK.
Zhang
H
H
Hancox
J C
JC
Kozlowski
R Z
RZ
D000368:Aged; D000838:Anions / Q000378:metabolism; D004553:Electric Conductivity; D005260:Female; D006325:Heart Atria / Q000166:cytology*; D006801:Humans; D008297:Male; D032342:Muscle Cells / Q000378:metabolism*; D018408:Patch-Clamp Techniques
D000838:Anions