Table 3.

Mean arterial diameter increases in AT arteries in response to flow with or without inhibitors

Artery	Absolute Change in Artery Diameter at Δ100 Flow Gradient ± SE, μm	Absolute Change in Artery Diameter at Δ100 Flow Gradient with Ba2+ ± SE, μm	Absolute Change in Artery Diameter at Δ100 Flow Gradient with l-NAME ± SE, μm
SAT-WT lean	35.5 ± 9.8	16.5 ± 10.0† (P = 0.037)	14.1 ± 12.3† (P = 0.040)
VAT-WT lean	43.3 ± 6.4	25.6 ± 4.0† (P = 0.021)	23.9 ± 5.9† (P = 0.031)
SAT-WT obese	47.6 ± 5.3	31.8 ± 8.8† (P = 0.044)	33.6 ± 11.3† (P = 0.046)
VAT-WT obese	26.7 ± 4.3* (P = 0.025)	24.8 ± 4.6	27.0 ± 9.4
SAT-CD36 KO lean	47.0 ± 2.6	27.2 ± 4.7† (P = 0.002)	25.9 ± 4.4† (P < 0.001)
VAT-CD36 KO lean	45.5 ± 6.3	28.7 ± 3.4† (P = 0.008)	31.4 ± 5.3† (P = 0.009)
SAT-CD36 KO obese	45.5 ± 4.8	32.8 ± 4.5† (P = 0.006)	35.8 ± 4.3† (P = 0.011)
VAT-CD36 KO obese	54.8 ± 6.9# (P = 0.014)	29.6 ± 2.7† (P = 0.003)	32.5 ± 1.7† (P = 0.008)

Mean increases in diameters in response to flow were assessed relative to the preconstricted diameter in each artery group. A two-way ANOVA followed by Bonferroni post hoc testes was used when comparing baseline diameters across diet and genotype (*significantly different vs. VAT-WT lean; #significantly different vs. VAT-WT obese). One-way repeated measures ANOVAs followed by bonferroni post hoc tests were used to determine the effects of inhibitors within each artery group (†significantly different vs. diameter changes in the absence of inhibitor within an artery group). AT, adipose tissue; SAT, subcutaneous adipose tissue; VAT, visceral adipose tissue; KO, knockout; WT; wild type; l-NAME, nitro-l-arginine methyl ester.