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Nitric oxide activates ATP‐dependent K + channels in human eosinophils
Author(s) -
Schwingshackl Andreas,
Moqbel Redwan,
Duszyk Marek
Publication year - 2002
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.71.5.807
Subject(s) - nitric oxide , patch clamp , endogeny , eosinophil , ion channel , biology , potassium channel , biophysics , in vivo , nitric oxide synthase , microbiology and biotechnology , biochemistry , pharmacology , endocrinology , immunology , receptor , asthma
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 (K ATP ). Although RT‐PCR studies showed the expression of several classes of K + channels in human eosinophils, NO donors affected only K ATP channel function. We conclude that NO, at concentrations likely to be encountered in vivo, could prevent eosinophil activation by opening K ATP channels.