Abstract
Superfusion of angiotensin II (Ang II) ceased blood flow in rat mesenteric microcirculation, however, successive reflow occurred. When nitric oxide synthase inhibitor was present, the stoppage of flow occurred by the lower concentration of Ang II. Superoxide dismutase (SOD) significantly delayed the stoppage by Ang II and restored the successive reflow earlier. The acute reaction between Ang II and mesenteric artery induced immediate superoxide (O(2)(-)) production when observed by a chemiluminescence method using the Cypridina luciferin analog. The acute vascular O(2)(-) production on the addition of Ang II contributed to in vitro vascular contraction as it was significantly attenuated by SOD. The acute superoxide-producing effect is likely to be specific to Ang II because such significant modification by SOD was not observed for norepinephrine.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Angiotensin II / metabolism*
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Angiotensin II / pharmacology*
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Animals
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Arginine / pharmacology
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Enzyme Inhibitors / pharmacology
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Imidazoles
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Luminescent Measurements
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Male
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Mesenteric Arteries / physiology
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Microcirculation / drug effects
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Microcirculation / physiology
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NG-Nitroarginine Methyl Ester / pharmacology
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Nitric Oxide / metabolism
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Norepinephrine / pharmacology
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Oxygen / blood
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Pyrazines
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Rats
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Rats, Inbred WKY
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Splanchnic Circulation / drug effects
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Splanchnic Circulation / physiology*
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Superoxide Dismutase / pharmacology
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Superoxides / metabolism*
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Vasoconstriction / drug effects
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Vasoconstrictor Agents / pharmacology
Substances
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Enzyme Inhibitors
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Imidazoles
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Pyrazines
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Vasoconstrictor Agents
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Superoxides
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Angiotensin II
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2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo(1,2-alpha)pyrazin-3-one
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Nitric Oxide
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Arginine
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Superoxide Dismutase
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Oxygen
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NG-Nitroarginine Methyl Ester
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Norepinephrine