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Contribution of nitric oxide to cutaneous microvascular dilation in individuals with type 2 diabetes mellitus

Departments of ¹Physiology and Biomedical Engineering, ²Anesthesiology, and ³Endocrinology, Mayo Clinic College of Medicine, Rochester, Minnesota

Submitted 21 July 2006 ; accepted in final form 30 August 2006

Microvascular pathophysiology associated with type 2 diabetes mellitus (T2DM) contributes to several aspects of the morbidity associated with the disease. We quantified the contribution of nitric oxide (NO) to the cutaneous vasodilator response to nonpainful local warming in subjects with T2DM (average duration of diabetes mellitus 7 ± 1 yr) and in age-matched control subjects. We measured skin blood flow in conjunction with intradermal microdialysis of N^G-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor) or vehicle during 35 min of local warming to 42°C. Microdialysis of sodium nitroprusside (SNP) was used for assessment of maximum cutaneous vascular conductance (CVC). Resting CVC was higher in T2DM subjects at vehicle sites (T2DM: 19 ± 2 vs. control: 11 ± 3%maxCVC; P < 0.05); this difference was abolished by L-NAME (T2DM: 10 ± 1 vs. control: 8 ± 1%maxCVC; P > 0.05). The relative contribution of NO to the vasodilator response to local warming was not different between groups (T2DM: 46 ± 4 vs. control: 44 ± 6%maxCVC; P > 0.05). However, absolute CVC during local warming was 25% lower in T2DM subjects (T2DM: 1.79 ± 0.15 AU/mmHg; controls: 2.42 ± 0.20 AU/mmHg; P < 0.01), and absolute CVC during SNP was 20% lower (T2DM: 1.91 ± 0.12 vs. control: 2.38 ± 0.13 AU/mmHg; P < 0.01). We conclude that the relative contribution of NO to vasodilation during local warming is similar between subjects with T2DM and control subjects, although T2DM was associated with a lower absolute maximum vasodilation.

skin blood flow; vasodilation; local warming; thermoregulation

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