Vasodilation and NO_x (nitrate/nitrite) production of coronary and skeletal muscular small arteries were induced by the mechanical or pharmacological stimulations. (A) Vasodilation of coronary small arteries was induced by the cyclic transmural pressure or stimulated by BK, ACh, or SNP after the treatments. (B) Vasodilation of skeletal muscular small arteries was induced by the cyclic transmural pressure or stimulated by BK, ACh, or SNP after the treatments. (C) NO_x production of coronary small arteries was exposed to stimulations after treatments. (D) NO_x production of skeletal muscular small arteries was exposed to stimulations after treatments. The treatments included intact and untreated vessel (IUT), isovolumic condition (IVC) to maintain the diameter constant during cyclic transmural pressure, L-NAME incubation (L-NA), endothelial cells mechanically removed using a wire (D-ECs), GRGDSP peptide incubation (RGD), GRGESP peptide incubation (RGE), incubation with function-blocking integrin α₅β₁ antibody (α₅β₁), incubation with function-blocking integrin α_vβ₃ antibody (α_vβ₃), and incubation with function-blocking integrin α₅β₁ and α_vβ₃ antibodies (2ABs). The number of the vessel segments in the various groups was as follows: coronary segments: n = 15 for IUT, n = 6 for L-NA, n = 5 for D-ECs, n = 6 for RGD, n = 6 for RGE, n = 5 for IVC, n = 6 for α₅β₁, n = 5 for α_vβ₃, and n = 11 for 2ABs; skeletal muscular vessel segments: n = 10 for IUT, n = 5 for L-NA, n = 5 for D-ECs, n = 6 for RGD, n = 5 for RGE, n = 4 for IVC, n = 6 for α₅β₁, n = 6 for α_vβ₃, and n = 10 for 2ABs. *, P < 0.05 versus incubations; #, P < 0.05 versus stimulations. Error bars represent mean ± SD.