Chronic inhibition of nitric oxide synthesis in rats increases aortic superoxide anion production via the action of angiotensin II

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Structured PICO

Population

Rat model (aortas of control rats and others receiving L-NAME)

Intervention

L-NAME (Nomega-nitro-L-arginine methyl ester) or L-NAME plus an angiotensin II type 1 receptor antagonist (CS-866) for 7 days

Comparator

Control rats

Outcome

Superoxide anion (O2-) production and activity of redox-sensitive transcription factors (NF-kappaB and AP-1) in aortassurrogate

Chronic inhibition of NO synthesis increases vascular oxidative stress via angiotensin II type 1 receptors, independent of hypertension.

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AT1 blockade may curb NO-deficiency oxidative stress independent of BP; hypothesis-generating in animals and leaves open human translation.

Kitamoto et al. (2000) studied this question.

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AT1 blockade may curb NO-deficiency oxidative stress independent of BP; hypothesis-generating in animals and leaves open human translation.