Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine β-synthase-deficient mice

• DOI: 10.1152/ajpheart.2000.279.3.h970
• Publication Date: 2017-12-22T08:26:22Z
• Authors: Steven R. Lentz; Rochelle A. Erger; Sanjana Dayal; Nobuyo Maeda; M. René Malinow; Donald D. Heistad; Frank M. Faraci
• Keywords: Hyperhomocysteinemia; Sodium nitroprusside; Endothelial Dysfunction; Homocystinuria; Transsulfuration

Hyperhomocysteinemia is a risk factor for stroke, myocardial infarction, and venous thrombosis. Moderate hyperhomocysteinemia associated with impaired endothelial function, but the mechanisms responsible dysfunction in are poorly understood. We have used genetic dietary approaches to produce mice. Heterozygous cystathionine beta-synthase-deficient mice (CBS +/-), which selective defect homocysteine transsulfuration, wild-type +/+) littermates were fed either control diet or that relatively deficient folic acid 6 wk. Plasma total was 5.3 +/- 0.7 microM CBS +/+ 6.4 0.6 (P = 0.3) given diet. 11.6 4.5 25.1 3.2 0.004) low-folate In diet, relaxation of aortic rings response endothelium-dependent vasodilator acetylcholine did not differ significantly between contrast, maximal markedly (58 9%) compared (84 4%) 0.01). No differences endothelium-independent sodium nitroprusside observed among four groups These data indicate CBS-deficient predisposed during folate deficiency, moderate marked impairment function