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Department of Physiology, New York Medical College, Valhalla, New York 10595
The inhibitor of soluble guanylate cyclase (sGC)
stimulation by nitric oxide (NO),
1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), was examined for its effects on the prolonged relaxation of
endothelium-removed bovine coronary (BCA) and pulmonary (BPA) arteries
to peroxynitrite (ONOO
)
and on
H2O2-elicited
relaxation and sGC stimulation. Our previous studies suggest that
ONOO causes a prolonged
relaxation of BPA by regenerating NO and that a 2-min exposure of BCA
or BPA to 50 nM NO causes an
ONOO-elicited relaxation.
The relaxation of K+-precontracted
BCA to 50 nM NO or 100 µM
ONOO was essentially
eliminated by 10 µM ODQ. ODQ also eliminated relaxation to 0.1 nM-10
µM of NO donor
S-nitroso-N-acetyl-penicillamine (SNAP), but it did not alter relaxation to 1-300 µM
H2O2.
Similar responses were also observed in BPA. ODQ did not increase
lucigenin-detectable superoxide production in BCA, and it did not alter
luminol-detectable endogenous
ONOO formation observed
during a 2-min exposure of BCA to 50 nM NO. In addition, ODQ did not
affect tissue release of NO after 2 min exposure of BCA to 50 nM NO.
The activity of sGC in BPA homogenate that is stimulated by endogenous
H2O2
was not altered by ODQ, whereas sGC activity in the presence of 10 µM
SNAP (+fungal catalase) was reduced by ODQ. Thus relaxation of
K+-precontracted BCA and BPA to
ONOO appears to be
completely mediated by NO stimulation of sGC, whereas the actions of
ODQ suggest that NO is not involved in
H2O2-elicited relaxation and sGC stimulation. This study did not detect evidence for
the participation of additional mechanisms potentially activated by
ONOO in the responses studied.
hydrogen peroxide; nitric oxide; redox signalling
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