Figure 5. EDH-type vasorelaxation is inhibited by gap junction inhibitors but unaffected by other putative modulators of the EDH.

A, mean acetylcholine-induced relaxation of noradrenaline-precontracted arteries (n= 4) in CO₂/HCO₃⁻-containing PSS under control conditions or treated with 30 μmol l⁻¹ Ba²⁺ to inhibit K_ir channels. B, average relaxation to 3 μmol l⁻¹ acetylcholine of noradrenaline-precontracted arteries (n= 4) in CO₂/HCO₃⁻-containing PSS under control conditions or treated with 100 nmol l⁻¹ iberiotoxin to inhibit BK channels. C, mean relaxation to 3 μmol l⁻¹ acetylcholine of noradrenaline-precontracted arteries (n= 4) in CO₂/HCO₃⁻-containing PSS under control conditions or treated with 250 U ml⁻¹ of the H₂O₂ scavenger PEG-catalase. D, mean relaxation to 3 μmol l⁻¹ acetylcholine of noradrenaline-precontracted arteries (n= 4) in CO₂/HCO₃⁻-containing PSS under control conditions or treated with 100 μmol l⁻¹ of the gap junction inhibitor carbenoxolone. E, mean relaxation of noradrenaline-precontracted arteries to acetylcholine (n= 4) in CO₂/HCO₃⁻-containing PSS under control conditions or treated with 30 μmol l⁻¹ of the gap junction inhibitor 18β-glycyrrhetinic acid. F, mean acetylcholine-induced relaxation of noradrenaline-precontracted arteries (n= 4) in the presence and absence of CO₂/HCO₃⁻ under control conditions or treated with 1 mmol l⁻¹ 8Br-cAMP. The effect of omitting or restoring CO₂/HCO₃⁻ was investigated 30 min after the buffer change to allow a new steady-state pH_i to be reached. Comparisons in A, E and F were performed by two-way ANOVA followed by Bonferroni post-hoc tests. Comparisons in B, C and D were performed by paired Student's t test. *P < 0.05, **P < 0.01 vs. CO₂/HCO₃⁻. NS, not significantly different from CO₂/HCO₃⁻ or as indicated.