Figure 6. Vasorelaxation to cholinergic stimulation is attenuated in arteries with PVT due to abolished H₂S production .

Vasorelaxant responses to ACh (A) (n = 6–13) and methacholine (B) (n = 5–17) were attenuated in U46619‐preconstricted arteries with PVT around the whole (1/1) or half (1/2) of the arterial circumference compared to arteries without PVT. C,original traces of vasorelaxant responses to cumulative application of methacholine in U46619‐preconstricted coronary septal arteries with and without PVT. At each arrow, the concentration of methacholine was increased by a half‐log step (between 10 nm and 10 μm). D and E,in the presence of 100 μm NO‐synthase inhibitor l‐NAME, the vasorelaxant response to methacholine was still significantly smaller in U46619‐preconstricted arteries with PVT compared to arteries without PVT. The l‐NAME‐insensitive vasorelaxant response to methacholine was sensitive to 10 mm CSE inhibitor PPG (D) (n = 6–8) and 10 μm K_v7 channel inhibitor XE991 (E) (n = 7–8). F,incubation with 10 mm CSE inhibitor PPG alone significantly attenuated the difference in vasorelaxation to methacholine stimulation between arteries with and without PVT (n = 14). G,vasorelaxation to methacholine in the presence of 1 μm PKC inhibitor Bis‐10 was persistently reduced in U46619‐preconstricted arteries with PVT compared to arteries without PVT (n = 8). Data were fitted to sigmoidal curve fits and compared using extra sum‐of‐squares F tests. Effects of pharmacological inhibitors on the methacholine responses were evaluated by comparing areas under the curves. **P < 0.01, ***P < 0.001. NS, not significantly different vs. arteries without PVT under the same conditions.