Superfusion of angiotensin II (Ang It) ceased blood flow in rat mesenteric
microcirculation, however, successive reflow occurred. When nitric oxide sy
nthase inhibitor was present, the stoppage of flow occurred by the lower co
ncentration of Ang II. Superoxide dismutase (SOD) significantly delayed the
stoppage by Ang II and restored the successive reflow earlier. The acute r
eaction 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 a
ddition of Ang II contributed to in vitro vascular contraction as it was si
gnificantly attenuated by SOD. The acute superoxide-producing effect is lik
ely to be specific to Ang Il because such significant modification by SOD w
as not observed for norepinephrine.