Superoxide production and oxygen consumption in endothelium-intact and -denuded artery stimulated by angiotensin II.

Arteries stimulated by angiotensin II (AII) to contract do not display the expected augmentation of O2 consumption seen with other cardiovascular contractile agonists. We tested the hypothesis that superoxide (O2-) or other reactive oxidant species generated by AII played a role in the paradoxical O2 consumption response in porcine carotid artery, with or without an intact endothelium. Endothelium-denuded arteries were incubated with either 1 microM diphenylene iodonium (DPI), an inhibitor of NAD(P)H oxidase, 300 u/ml superoxide dismutase (SOD), a scavenger of O2-, or 20 U/ml catalase, an enzyme which promotes conversion of O2- (scavenged in the form of H2O2) to O2. DPI treatment resulted in the expected increase in O2 consumption upon contractile activation with AII challenge (1.05+/- 0.23 micromol/g/min; n = 6, p < .01), as did treatment with SOD (0.67+/- 0.20 micromol/g/min; n = 4, p < .05). Catalase incubation resulted in a burst of O2 generation upon AII challenge (1.30 +/- 0.21 micromol/g/min; n = 10, p < .001). In endothelium-intact arteries, O2 consumption was again not augmented with AII challenge; instead, a burst of O2 production was observed (0.66 +/- 0.22 micromol/g/min; n = 9, p < .05), which was not affected further by addition of catalase. Thus, the absence of apparent augmentation of O2 consumption during contractile activation of endothelium-denuded arteries was attributed to simultaneous NAD(P)H oxidase-dependent production of O2-, and attendant H2O2 and O2 generation which either and masked the detection of O2 consumed or suppressed mitochondrial uptake of O2, or both. An intact endothelium was required to manifest the burst of O2 generation with AII stimulation under normal conditions.