In spontaneously hypertensive rats, impaired nitric oxide bioavailability in the kidney is driven by ANG II-mediated superoxide production via NAD(P)H oxidase overexpression and loss of SOD-3.
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Oxidative stress may impair renal NO effects in hypertensive rat models; hypothesis-generating for human hypertension therapies.
Adler et al. (2004) studied this question.
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