Effect of sodium nitrite supplementation on endothelial dysfunction in diabetic mice

Abstract

Nitrite is an oxidative breakdown product of nitric oxide that has been shown to restore cardiovascular dysfunction in various settings, although its effects on diabetes‐related endothelial dysfunction are unclear. We therefore tested the hypothesis that short‐term nitrite therapy restores endothelial dysfunction in diabetic mice. Genetically obese, diabetic mice (db/db) were administered drinking water with or without sodium nitrite (50 mg/‐L) for 4 weeks. Isolated carotid arteries of diabetic mice had lower acetylcholine (ACh)‐induced endothelium‐dependent dilation (EDD) compared to heterozygous control mice (db/+) (71.2 ±14.3% vs. 93±7.0%; p<0.05). Sodium nitrite supplementation restored EDD to control levels (92.9±2.3% vs. 93±7.0%; p<0.05). Sodium Nitroprusside (SNP)‐induced endothelium‐independent dilation did not differ between diabetic and control mice (99.8±4.2% vs. 97.2±4.2%; p<0.05) or following nitrite supplementation (99.8±1.2%; p<0.05). These data suggest that sodium nitrite may be a novel therapy for treating diabetes‐related arterial dysfunction.5 K01 DK087777‐03 PI: Gentile, Christopher, NIH AG013038 PI: Douglas R. Seals