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Asthma Research Group, Smooth Muscle Research Group, Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5
We
compared the effects of two redox forms of nitric oxide,
NO+ [liberated by
S-nitroso-N-acetyl-penicillamine (SNAP)] and
NO · [liberated by 3-morpholinosydnonimine (SIN-1) in
the presence of superoxide dismutase], on cytosolic concentration
of Ca2+ ([Ca2+]i;
single cells) and tone (intact strips) obtained from human main stem
bronchi and canine trachealis. SNAP evoked a rise in [Ca2+]i that was unaffected by
removing external Ca2+ but was markedly reduced by
depleting the internal Ca2+ pool using cyclopiazonic acid
(10
5 M). Dithiothreitol (1 mM) also
antagonized the Ca2+ transient as well as the accompanying
relaxation. SNAP attenuated responses to 15 and 30 mM KCl but not those
to 60 mM KCl, suggesting the involvement of an electromechanical
coupling mechanism rather than a direct effect on the contractile
apparatus or on Ca2+ channels. SNAP relaxations were
sensitive to charybdotoxin (107 M) or
tetraethylammonium (30 mM) but not to 4-aminopyridine (1 mM).
Neither SIN-1 nor 8-bromoguanosine 3',5'-cyclic
monophosphate had any significant effect on resting
[Ca2+]i, although both of these
agents were able to completely reverse tone evoked by carbachol
(107 M). We conclude that
NO+ causes release of internal Ca2+ in a
cGMP-independent fashion, leading to activation of
Ca2+-dependent K+ channels and relaxation,
whereas NO · relaxes the airways through a cGMP-dependent,
Ca2+-independent pathway.
Ca2+-dependent K+ channels; redox forms of nitric oxide; electromechanical coupling
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