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Research Article Free access | 10.1172/JCI118394

Vitamin C improves endothelium-dependent vasodilation in patients with non-insulin-dependent diabetes mellitus.

H H Ting, F K Timimi, K S Boles, S J Creager, P Ganz, and M A Creager

Vascular Medicine and Atherosclerosis Unit, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Ting, H. in: JCI | PubMed | Google Scholar

Vascular Medicine and Atherosclerosis Unit, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Timimi, F. in: JCI | PubMed | Google Scholar

Vascular Medicine and Atherosclerosis Unit, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

Find articles by Boles, K. in: JCI | PubMed | Google Scholar

Vascular Medicine and Atherosclerosis Unit, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

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Vascular Medicine and Atherosclerosis Unit, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

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Vascular Medicine and Atherosclerosis Unit, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.

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Published January 1, 1996 - More info

Published in Volume 97, Issue 1 on January 1, 1996
J Clin Invest. 1996;97(1):22–28. https://doi.org/10.1172/JCI118394.
© 1996 The American Society for Clinical Investigation
Published January 1, 1996 - Version history
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Abstract

Endothelium-dependent vasodilation is impaired in humans with diabetes mellitus. Inactivation of endothelium-derived nitric oxide by oxygen-derived free radicals contributes to abnormal vascular reactivity in experimental models of diabetes. To determine whether this observation is relevant to humans, we tested the hypothesis that the antioxidant, vitamin C, could improve endothelium-dependent vasodilation in forearm resistance vessels of patients with non-insulin-dependent diabetes mellitus. We studied 10 diabetic subjects and 10 age-matched, nondiabetic control subjects. Forearm blood flow was determined by venous occlusion plethysmography. Endothelium-dependent vasodilation was assessed by intraarterial infusion of methacholine (0.3-10 micrograms/min). Endothelium-independent vasodilation was measured by intraarterial infusion of nitroprusside (0.3-10 micrograms/min) and verapamil (10-300 micrograms/min). Forearm blood flow dose-response curves were determined for each drug before and during concomitant intraarterial administration of vitamin C (24 mg/min). In diabetic subjects, endothelium-dependent vasodilation to methacholine was augmented by simultaneous infusion of vitamin C (P = 0.002); in contrast, endothelium-independent vasodilation to nitroprusside and to verapamil were not affected by concomitant infusion of vitamin C (P = 0.9 and P = 0.4, respectively). In nondiabetic subjects, vitamin C administration did not alter endothelium-dependent vasodilation (P = 0.8). We conclude that endothelial dysfunction in forearm resistance vessels of patients with non-insulin-dependent diabetes mellitus can be improved by administration of the antioxidant, vitamin C. These findings support the hypothesis that nitric oxide inactivation by oxygen-derived free radicals contributes to abnormal vascular reactivity in diabetes.

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