Circulation. 2002;106:987-992
Published online before print July 29, 2002, doi: 10.1161/01.CIR.0000027109.14149.67
Published online before print July 29, 2002, doi: 10.1161/01.CIR.0000027109.14149.67
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(Circulation. 2002;106:987.)
© 2002 American Heart Association, Inc.
Basic Science Reports |
Impaired Nitric Oxide Synthase Pathway in Diabetes Mellitus
Role of Asymmetric Dimethylarginine and Dimethylarginine Dimethylaminohydrolase
From the Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, Calif (K.Y.L., A.I., T.A., P.S.T., S.A., G.M.R., J.P.C.), and the Department of Nutritional Science, Okayama Prefectural University, Soja, Okayama, Japan (M.K., H.T.).
Correspondence to John P. Cooke, MD, PhD, Division of Cardiovascular Medicine, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA 94305. E-mail john.cooke{at}stanford.edu
Background— An endogenous inhibitor of nitric oxide synthase, asymmetric dimethylarginine (ADMA), is elevated in patients with type 2 diabetes mellitus (DM). This study explored the mechanisms by which ADMA becomes elevated in DM.
Methods and Results— Male Sprague-Dawley rats were fed normal chow or high-fat diet (n=5 in each) with moderate streptozotocin injection to induce type 2 DM. Plasma ADMA was elevated in diabetic rats (1.33±0.31 versus 0.48±0.08 µmol/L; P<0.05). The activity, but not the expression, of dimethylarginine dimethylaminohydrolase (DDAH) was reduced in diabetic rats and negatively correlated with their plasma ADMA levels (P<0.05). DDAH activity was significantly reduced in vascular smooth muscle cells and human endothelial cells (HMEC-1) exposed to high glucose (25.5 mmol/L). The impairment of DDAH activity in vascular cells was associated with an accumulation of ADMA and a reduction in generation of cGMP. In human endothelial cells, coincubation with the antioxidant polyethylene glycol–conjugated superoxide dismutase (22 U/mL) reversed the effects of the high-glucose condition on DDAH activity, ADMA accumulation, and cGMP synthesis.
Conclusions— A glucose-induced impairment of DDAH causes ADMA accumulation and may contribute to endothelial vasodilator dysfunction in DM.
Key Words: nitric oxide • endothelium • oxidative stress
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 M. Knipp, O. Braun, P. M. Gehrig, R. Sack, and M. Vasak Zn(II)-free Dimethylargininase-1 (DDAH-1) Is Inhibited upon Specific Cys-S-Nitrosylation J. Biol. Chem., January 24, 2003; 278(5): 3410 - 3416. [Abstract] [Full Text] [PDF]
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