The diabetic (DM) or non-diabetic (ND) microvessels were pre-constricted with the thromboxane A2 analog U46619 to reach a 30%-40% reduction of the baseline diameter. After a stable constriction, microvascular relaxation in response to the SK activator NS309 (0-10μM); (A), ADP (10μM); (B); and (C) SNP(100μM) in the presence or absence of MT (0-10μM) was measured. ND(H/R) = ND treated by hypoxia/re-oxygenation; ND(H/R)+1μM MT = ND(H/R) + 1μM mito-Tempo; ND(H/R)+10μM MT = ND(H/R) + 10 μM mito-Tempo; DM(H/R) = DM treated by hypoxia/re-oxygenation; DM(H/R) +1μM MT = DM(H/R) + 1μM mito-Tempo; DM(H/R) +10μM MT = DM(H/R) + 10μM mito-Tempo; n= 5-6/group; A, @P =0.0002, ND(H/R) vs. DM(H/R); *P= 0.002 , ND(H/R) + 10μM MT vs. ND (H/R) #P = 0.0329, DM(H/R) + 10μM MT vs. DM(H/R); $P <0.0001, ND(H/R) +10μM MT vs. DM(H/R) +10μM MT; B, @P <0.0001, ND(H/R) vs. DM(H/R); *P = 0.0438, ND(H/R) + 10μM MT vs. ND (H/R); #P =0.0293, DM(H/R) + 10μM MT vs. DM(H/R); $P <0.0001, ND(H/R) +10μM MT vs. DM(H/R) +10μM MT; Mean ± SD, Two-way ANOVA with a post hoc Bonferroni test.