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1 Department of Physiology, New York Medical College, Valhalla, New York 10595; and 2 Division of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan 48202
Flow-induced
dilation was examined in isolated coronary arteries of
endothelial nitric oxide (NO) synthase knockout mice (eNOS-KO) and
wild-type (WT) mice. The basal tone of arteries (percentage of passive
diameter) was significantly greater in eNOS-KO than in WT mice; their
flow-induced dilations, however, were similar. Endothelial removal
eliminated the dilations in vessels of both strains of mice. In
arteries of WT mice,
N
-nitro-L-arginine methyl
ester (L-NAME) (10
4 M) or indomethacin
(105 M) alone, inhibited flow-induced dilation by
~50%, whereas their simultaneous administration abolished the
responses. In arteries of eNOS-KO mice, flow-induced dilation was
inhibited by ~40% with L-NAME. The residual portion
(60%) of the response was eliminated by the additional administration
of indomethacin. 7-Nitroindazole (104 M) attenuated
flow-induced dilation by ~40% in arteries of eNOS-KO mice, but did
not affect responses in those of WT mice.
1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (3 × 105 M) inhibited the
L-NAME/7-nitroindazole-sensitive portion of the responses
in arteries of eNOS-KO mice. Immunohistochemical evidence confirms the
presence of neuronal NOS (nNOS) in the arterial endothelium of eNOS-KO
mice. In conclusion, nNOS-derived NO, via activation of cGMP, together
with prostaglandins, maintains flow-induced dilation in coronary
arteries of male eNOS-KO mice.
endothelial nitric oxide; prostaglandins; flow-induced dilation
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