Figure 3. Effects of various pharmacologic inhibitors on the ACh (3 micro Meter)-induced hyperpolarization in the endothelium-intact strips. (A) The effects of various inhibitors of EDRF pathway on the ACh hyperpolarization. (a-d) Typical examples of the effects of N^G-nitro L-arginine (LNNA, 100 micro Meter), oxyhemoglobin (HbO², 10 micro Meter), methylene blue (MB, 10 micro Meter), and a cocktail application of LNNA (100 micro Meter), HbO²(10 micro Meter), and MB (10 micro Meter) on the hyperpolarization. (e) Effects of these EDRF inhibitors on the resting membrane potential and the effects of ACh on the membrane potential in the presence of the EDRF inhibitors. Data are mean + SD (n = 5–9). *Significantly different (P < 0.05) from the membrane potential before application of ACh either in the absence or presence of EDRF inhibitors. #Significantly different (P < 0.05) from the control membrane potential before application of the EDRF inhibitors. NS = not significantly different from the control membrane potential before application of the EDRF inhibitors. (B) Effects of various Potassium channel blockers on the ACh hyperpolarization. (a-d) Typical examples of the effects of glibenclamide (Glib, 10 micro Meter), BaCl²(100 micro Meter), 4-aminopyridine (4AP, 100 micro Meter), and apamin (0.3 micro Meter) on the hyperpolarization. (e) Effects of various Potassium sup + channel blockers on the resting membrane potential and the effects of ACh on the membrane potential in the presence of these Potassium sup + channel blockers. Data are mean plus/minus SD (n = 5–11, three to four preparations). *Significantly different (P < 0.05) from the control membrane potential before application of ACh either in the absence or presence of Potassium sup + channel blockers. #Significantly different (P < 0.05) from the control membrane potential before application of the Potassium sup + channel blockers. NS = not significantly different from the control membrane potential before application of the Potassium sup + channel blockers.