VITAMIN-E AMELIORATES THE RENAL INJURY OF DAHL SALT-SENSITIVE RATS

Recently, hyperlipidemia as well as hypertension has been observed in Dahl salt-sensitive (S) rats. In this study, to investigate whether th e lipid abnormality is involved in the renal injury of Dahl S rats, we examined the effect of vitamin E on glomerular sclerosis, as vitamin E is an inhibitor of lipid oxidation. Dahl S rats were given a high sa lt diet (8% NaCl) containing either normal vitamin E (2 mg/100 g) or h igh vitamin E (50 mg/100 g) for 4 weeks. Dahl salt-resistant (R) rats were given a high salt and normal vitamin E diet. The blood pressure i n the Dahl rats increased and was not suppressed by the vitamin E supp lement. Serum cholesterol and triglycerides in Dahl S rats were higher than in Dahl R rats at both 0 and 4 weeks. Vitamin E lowered the seru m cholesterol level in Dahl S rats at 4 weeks (126 +/- 5 v 150 +/- 12 mg/dL, P < .01). Urinary protein excretion and serum creatinine increa sed in Dahl S rats, and vitamin E inhibited the increases significantl y (urinary protein, 70.7 +/- 0.9 v 178.0 +/- 8.8 mg/day, P < .01; seru m creatinine, 0.45 +/- 0.02 v 0.63 +/- 0.05 mg/dL, P < .01). Serum lip id peroxide (LPO) was higher in Dahl S rats than in Dahl R rats, and v itamin E lowered LPO in Dahl S rats (2.10 +/- 0.03 v 2.70 +/- 0.04 nmo l/ml, P < .01). In the histologic study, sclerosing score (SS) of glom eruli, which represents the degree of glomerulosclerosis semiquantitat ively, was higher in Dahl S rats than in Dahl R rats. Vitamin E lowere d SS (114 +/- 3 v 157 +/- 6, P < .01) and ameliorated arterial injurie s such as medial thickness with partial necrosis and severe fibrinoid proliferation with inflammatory cell infiltration. In all rats, SS was strongly correlated with urinary protein (r = 0.93, P < .01), serum c holesterol (r = 0.86, P < .01), and serum LPO (r = 0.89, P < .01). The se results suggest that the renal injury in Dahl S rats is caused not only by hypertension but also by hyperlipidemia. Therefore, vitamin E might ameliorate the renal damage by inhibiting the oxidation of lipid s. (C) 1997 American Journal of Hypertension, Ltd.