Journal of Leukocyte Biology eBioscience full spectrum cell analysis
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(Journal of Leukocyte Biology. 2002;71:807-812.)
© 2002 by Society for Leukocyte Biology

Nitric oxide activates ATP-dependent K+ channels in human eosinophils

Andreas Schwingshackl*, Redwan Moqbel{dagger} and Marek Duszyk*

Departments of
* Physiology and
{dagger} Medicine, Pulmonary Research Group, University of Alberta, Edmonton, Canada

Correspondence: Dr. Marek Duszyk, Department of Physiology, University of Alberta, 7-46 Medical Sciences Building, Edmonton, Alberta T6G 2H7, Canada. E-mail: marek.duszyk{at}ualberta.ca

Nitric oxide (NO) affects the function of ion channels in many cell types, but its role in the regulation of eosinophil ion channels is unknown. In this study, we used the perforated patch-clamp method to investigate the effect of endogenous and exogenous NO on eosinophil ion channels. Using the NO synthase inhibitor, N-nitro-L-arginine methyl ester, we showed that endogenous NO did not affect the whole-cell current in eosinophil. However, two NO donors, S-nitroso-glutathione and S-nitroso-N-acetyl penicillamine, activated whole-cell currents via a NO/cGMP-dependent pathway. Ion substitution and pharmacological studies showed that NO-activated currents were carried by K+ ions, likely through ATP-dependent K+ channels (KATP). Although RT-PCR studies showed the expression of several classes of K+ channels in human eosinophils, NO donors affected only KATP channel function. We conclude that NO, at concentrations likely to be encountered in vivo, could prevent eosinophil activation by opening KATP channels.

Key Words: cGMP • diazoxide • KATP • RT-PCR






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