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• W2089125418 abstract "Bradykinin, a potent vasodilator, stimulates the formation of reactive oxygen species and F2-isoprostanes in vitro. The effect of bradykinin on oxidative stress in humans is not known. This study tested the hypothesis that bradykinin induces oxidative stress through a nitric oxide (NO)-dependent mechanism in the human vasculature. We measured forearm blood flow (FBF) and net F2-isoprostane release in response to intraarterial bradykinin (50–200 ng/min), nitroprusside (1.6–6.4 µg/min), or diltiazem (3.6–14.4 µg/min) in the absence and presence of the NO synthase inhibitor Nω-monomethyl-L-arginine (L-NMMA) in normotensive and hypertensive subjects pretreated with aspirin. L-NMMA significantly decreased basal FBF and basal net F2-isoprostane release (from 28.7 ± 5.2 to 13.4 ± 3.5 pg/min/100 ml, P = 0.01) in all subjects. Bradykinin caused a significant increase in FBF and net F2-isoprostane release in both normotensive and hypertensive subjects. During NO synthase inhibition, bradykinin significantly increased net F2-isoprostane release in both groups (P = 0.001) and there was no effect of L-NMMA on bradykinin-stimulated F2-isoprostane release (P = 0.46). Nitroprusside also significantly increased net F2-isoprostane release in hypertensive subjects (P = 0.01) and this response was not affected by L-NMMA (P = 0.50). Diltiazem increased FBF as well as net F2-isoprostane release (from 44.5 ± 12.5 to 61.2 ± 14.7 pg/min/100 ml at the highest dose, P = 0.05). Increasing blood flow induces oxidative stress through a NO- and endothelium-independent mechanism." @default.
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• W2089125418 date "2010-07-01" @default.
• W2089125418 modified "2023-09-26" @default.
• W2089125418 title "Increased blood flow induces oxidative stress through an endothelium- and nitric oxide-independent mechanism" @default.
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• W2089125418 doi "https://doi.org/10.1016/j.freeradbiomed.2010.04.023" @default.
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