Investigation Into the Sources of Superoxide in Human Blood Vessels
Key result
Angiotensin II increases superoxide production ~73% in human internal mammary arteries vs control.
- 95% CI 336, 925
- P=0.0001
- n=27
Why the study?
Increased vascular superoxide anion production contributes to endothelial dysfunction and hypertension, but the sources and mechanisms in human blood vessels are unclear.
Population
Internal mammary arteries and saphenous veins collected at cardiac surgery (n=27)
Comparison
Incubation with Ang II and/or inhibitors versus control incubation
Design
Ex vivo experimental study measuring superoxide production in human vessels
Follow-up
4 hours
Authors
Discussion
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Member takes
Implication
May increase vascular oxidative stress via AT1/NAD(P)H oxidase in models; leaves open clinical relevance to human endothelial dysfunction.
Structured PICO
P
Population
Human internal mammary arteries and saphenous veins collected at the time of cardiac surgery for ex vivo analysis.
I
Intervention
Incubation with Angiotensin II (1 pmol/L to 1 micromol/L) and/or inhibitors (diphenyleneiodonium, allopurinol, losartan)
C
Comparator
Control (incubation without Ang II or inhibitors)
O
Outcome
Superoxide anion (.O(2)(-)) production measured by lucigenin chemiluminescencesurrogate
Main Result
Absolute Event Rate: 1690% vs 978%
p-value: p=0.0001
Angiotensin II increases superoxide production in human internal mammary arteries via an AT1 receptor-dependent mechanism involving NAD(P)H oxidase.
Cite This Study
Berry et al. (2000) studied Cardiovascular disease (patients undergoing cardiac surgery) (n=27). Angiotensin II vs. Control (absence of Angiotensin II) was evaluated on Superoxide production in internal mammary arteries (95% CI 336, 925, p=0.0001). Angiotensin II significantly increased superoxide production in human internal mammary arteries compared to control (1690 vs 978 pmol/min/mg; 95% CI 336-925; P=0.0001).