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Research Article Free access | 10.1172/JCI114464
Howard Hughes Medical Institute, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
Find articles by Krause, K. in: JCI | PubMed | Google Scholar
Howard Hughes Medical Institute, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
Find articles by Welsh, M. in: JCI | PubMed | Google Scholar
Published February 1, 1990 - More info
To investigate the regulation of membrane voltage and transmembrane ion fluxes in human neutrophils, we studied plasma membrane currents using the whole-cell patch-clamp method. We observed three distinct ion channel currents: (a) a voltage-dependent K+ current, (b) a Ca2(+)-activated K+ current, and (c) a Ca2(+)-activated Cl- current. The voltage-dependent K+ current was found in cells at rest. Its conductive properties suggested an inwardly rectifying channel. The channel was activated at membrane potentials more positive than -60 mV, suggesting that it may determine the resting membrane potential of neutrophils. Activation of neutrophils by the Ca2+ ionophore ionomycin led to an increase in whole-cell K+ and Cl- currents. The Ca2(+)-activated K+ channel differed from the voltage-dependent K+ channel because it was insensitive to voltage, because it rectified outwardly, and because the voltage-sensitive K+ channel was Ca2(+)-independent. The Ca2(+)-activated Cl- channel showed outward rectification and no apparent voltage dependency. The Ca2(+)-activated K+ and Cl- channels may play a role in cell volume homeostasis and/or cellular activation.