Key result
High-dose vitamin E ameliorated CRF-induced hypertension, improved vascular NO production, lowered tissue nitrotyrosine burden, and reversed downregulations of NOS isoforms in rats.
Why the study?
Does high-dose vitamin E antioxidant therapy improve hypertension and nitric oxide availability in a rat model of chronic renal failure?
Population
Male Sprague Dawley rats with induced chronic renal failure (5/6 nephrectomy) and sham-operated controls
Comparison
Antioxidant-fortified diet for 6 weeks vs Regular diet (vitamin E, 40 U/Kg food) for 6 weeks
Design
Preclinical, Rats were randomized to CRF and sham-operated controls and fed…
Follow-up
6 weeks
Authors
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Should not change clinical practice; hypothesis-generating for antioxidant therapy targeting NO pathways in CRF models.
RCT
randomized
Does high-dose vitamin E antioxidant therapy improve hypertension and nitric oxide availability in a rat model of chronic renal failure?
High-dose vitamin E ameliorates oxidative stress, enhances nitric oxide availability, and improves hypertension in a rat model of chronic renal failure.
Vaziri et al. (2002) conducted an RCT in Chronic renal failure. Antioxidant-fortified diet (vitamin E) vs. Regular diet (vitamin E, 40 U/Kg food) was evaluated on Blood pressure, plasma malondialdehyde (MDA), tissue NO synthase (NOS) isoforms, tissue nitrotyrosine, and vascular tissue NO production. High-dose vitamin E ameliorated CRF-induced hypertension, improved vascular NO production, lowered tissue nitrotyrosine burden, and reversed downregulations of NOS isoforms in rats.
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