Figure 3. The VSMC membrane potential is unaffected by PVT, and the anti‐contractile effect of PVT persists after inhibition of K⁺ channels, H₂S and NO synthesis and adenosine receptors .

A,original traces of matched VSMC membrane potential and arterial force development during serotonin stimulation. B,VSMC membrane potentials at rest and during stimulation with 1 μm serotonin or 1 μm U46619 did not differ between coronary septal arteries with and without PVT (n = 7–8). C,the anti‐contractile effect of PVT around coronary septal arteries (n = 8) persists in the presence of 10 μm K_ATP channel inhibitor glibenclamide. Resting tension prior to the addition of serotonin was 0.80 ± 0.09 N/m (No PVT) and 0.72 ± 0.09 N/m (1/2 PVT) in the presence of glibenclamide compared to 0.81 ± 0.09 N/m (No PVT) and 0.84 ± 0.10 N/m (1/2 PVT) without glibenclamide. D and E,the increase in basal arterial tension following the addition of 10 μm K_v7 channel inhibitor XE991 (D) (n = 11) or 1 μm BK channel inhibitor paxillin (E) (n = 6) was reduced in arteries with PVT compared to arteries without PVT. No further basal tone development was seen if the concentration of paxillin was increased to 10 μm (data not shown). Resting tension was 0.60 ± 0.04 N/m (No PVT) and 0.61 ± 0.07 N/m (1/2 PVT) prior to the addition of XE991, and 0.57 ± 0.06 N/m (No PVT) and 0.74 ± 0.04 N/m (1/2 PVT) prior to addition of paxillin. F,the vasocontractile responses to serotonin were unaffected by 10 mm CSE inhibitor PPG in coronary septal arteries with and without PVT (n = 8). The slight rightward shifts of the concentration–response curves were similar to effects observed in time control experiments without addition of drug. Resting tension prior to the addition of serotonin was 0.81 ± 0.12 N/m (No PVT) and 0.61 ± 0.04 N/m (1/2 PVT) in the presence of PPG compared to 0.67 ± 0.04 N/m (No PVT) and 0.64 ± 0.04 N/m (1/2 PVT) without PPG. G,the increase in basal arterial tension following the addition of 100 μM NO‐synthase inhibitor l‐NAME was reduced in arteries with PVT compared to arteries without PVT (n = 6). Resting tension prior to addition of l‐NAME was 0.74 ± 0.11 N/m (No PVT) and 0.73 ± 0.08 N/m (1/2 PVT). H,vasocontractile responses to serotonin were unaffected by 100 μm adenosine receptor antagonist 8‐SPT in coronary septal arteries with and without PVT (n = 5). Resting tension prior to the addition of serotonin was 0.62 ± 0.02 N/m (No PVT) and 0.36 ± 0.03 N/m (1/2 PVT) in the presence of 8‐SPT compared to 0.65 ± 0.03 N/m (No PVT) and 0.53 ± 0.02 N/m (1/2 PVT) without 8‐SPT. The data were compared by a paired two‐tailed Student's t test (B, D, E and G) or fitted to sigmoidal curve fits and compared using extra sum‐of‐squares F tests (C, F and H). **P < 0.01, ***P < 0.001. NS, not significantly different vs. arteries without PVT.