Figure 5. The effects of various inhibitors of the EDRF pathway inhibitors and tetraethylammonium (TEA) on the ACh-induced relaxation in the endothelium-intact strips precontracted with norepinephrine (NE, 10 micro Meter). (A) Examples of ACh (0.03–0.3 micro Meter)-induced endothelium-dependent relaxation in the absence of EDRF pathway inhibitors (control). (B) The effects of a cocktail application of NG-nitro L-arginine (LNNA, 100 micro Meter), oxyhemoglobin (HbO2, 10 micro Meter), and methylene blue (MB, 10 micro Meter) on the relaxation elicited by a low concentration of ACh (0.1 micro Meter). (C) The effects of TEA (10 mM) on the remaining ACh (3 micro Meter)-induced relaxation after application of the EDRF pathway inhibitors. (D) The effects of EDRF pathway inhibitors (100 micro Meter LNNA [L], 10 micro Meter MB [M], 10 micro Meter HbO2[H], and a cocktail application of 100 micro Meter LNNA, 10 micro Meter MB, and 10 micro Meter HbO2[L + M + H]) on the ACh (0.03–10 micro Meter)-induced vasorelaxation. The open circles show the control ACh relaxation in the absence of the inhibitors (control). The closed circles show the effects of the above interventions on the ACh relaxation. C = control, L = LNNA, NG-nitro L-arginine, M = MB, methylene blue, H - HbO2, oxyhemoglobin, LMH = L + M + H, a cocktail application of 100 micro Meter LNNA, 10 micro Meter MB, and 10 micro Meter HbO2. All data are mean plus/minus SD (n = 3–8). *Significantly different (P < 0.05) from the control ACh-induced relaxation at each concentration. #Significantly different (P < 0.05) from the control within each group (this symbol was not added to the control group). (section)Significantly different (P < 0.05) from the LMH group at each concentration.