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A comparative study of the protective effect of simvastatin and moxonidine against renovascular toxicity induced by smoking in rats
Author(s) -
Nasr Magda A,
Elgowilly Sahar M,
ElMas Mahmoud M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1129.11
Subject(s) - moxonidine , simvastatin , pharmacology , chemistry , malondialdehyde , creatinine , renal function , endocrinology , medicine , oxidative stress , agonist , receptor
Oxidative stress plays a major role in smoking‐induced renal injury. We conducted biochemical and functional studies to assess the protective effect of the lipid lowering drug simvastatin and the antihypertensive agent moxonidine against renovascular toxicity caused by smoking. Six groups of rats (n=8 each) were used: (i) control, (ii) cigarette smoke (CS, twice a day, 30 min each, 6 weeks), (iii) simvastatin (2×5 mg/kg/day, s.c), (iv) moxonidine (2×1 mg/kg/day, i.p.), (v) CS+simvastatin, and (vi) CS+moxonidine. CS exposure increased plasma urea and creatinine and renal malondialdyde and decreased renal glutathione peroxidase, superoxide dismutase and catalase activities. In the isolated perfused phenylephrine‐preconstricted kidney, CS attenuated vasodilator responses to carbachol or isoprenaline in contrast to no effect on papaverine vasodilation. Simvastatin or moxonidine treatment virtually abolished the deleterious effects of CS on lipid peroxidation, antioxidant activity, and urea and creatinine levels. Further, both protective drugs ameliorated the attenuating effect of smoking on carbachol renal vasodilations; isoprenaline vasodilation was improved only by moxonidine. Conclusions: while moxonidine and simvastatin are equipotent in correcting renal oxidative damage caused by smoking, moxonidine appears to be more effective in rectifying vascular reactivity abnormalities.