Journal of Applied Physiology AJP: Renal Physiology
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J Appl Physiol 106: 566-570, 2009. First published December 4, 2008; doi:10.1152/japplphysiol.91289.2008
8750-7587/09 $8.00
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Skin blood flow and nitric oxide during body heating in type 2 diabetes mellitus

Lynn A. Sokolnicki,1 Nicholas A. Strom,1,2 Shelly K. Roberts,1,2 Shirley A. Kingsley-Berg,1 Ananda Basu,3 and Nisha Charkoudian1,2

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

Submitted 26 September 2008 ; accepted in final form 26 November 2008

Individuals with type 2 diabetes mellitus (T2DM) often exhibit microvascular dysfunction that may contribute to impaired thermoregulation, but potential mechanisms remain unclear. Our goals were to quantify skin blood flow responses and nitric oxide-mediated vasodilation during body heating in individuals with T2DM compared with nondiabetic control subjects of similar age. We measured skin blood flow (laser-Doppler flowmetry) in conjunction with intradermal microdialysis of NG-nitro-L-arginine methyl ester (L-NAME; nitric oxide synthase inhibitor) or vehicle during 45–60 min of whole body heating (WBH) in 10 individuals with T2DM and 14 control subjects. In six individuals from each group, we also measured forearm blood flow (FBF) by venous occlusion plethysmography on the contralateral forearm. FBF responses showed diminished absolute cutaneous vasodilation during WBH in the T2DM group (PANOVA < 0.01; peak FBF in control 13.1 ± 1.7 vs. T2DM 9.0 ± 1.6 ml·100 ml–1·min–1). However, the relative contribution of nitric oxide to the cutaneous vasodilator response (expressed as % of maximal cutaneous vascular conductance) was not different between groups (P > 0.05). We conclude that cutaneous vasodilator responses to WBH are decreased in individuals with T2DM, but the contribution of nitric oxide to this smaller vasodilation is similar between T2DM and control individuals. This decrease in cutaneous vasodilation is likely an important contributor to impaired thermoregulation in T2DM.

metabolic diseases; microvasculature; heat stress; cutaneous circulation


Address for reprint requests and other correspondence: N. Charkoudian, Dept. of Physiology and Biomedical Engineering, JO 4-184W, Mayo Clinic College of Medicine, 200 First St. SW, Rochester, MN 55901 (e-mail: charkoudian.nisha{at}mayo.edu)






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