Figure 2.

Vasorelaxant effect of EEJ. Data are expressed as mean ± SD (n = 8). (a) Cumulative concentration response for EEJ (0.125, 0.25, 0.5, 1, and 2 g/L) on PE (10 μM) or KCl (60 mM) precontracted endothelium-intact thoracic aorta rings. Maximum contraction amplitude induced by PE (10 μM) is considered as 100%. (b) Effects of L-NAME (3 mM) and Indo (10 μM) on EEJ induced relaxation in the endothelium-intact aorta rings precontracted with PE (10 μM). ^* P < 0.05,^** P < 0.01 compared with control group. (c) Effects of 4-AP (5 mM), BaCl₂ (1 mM), TEA (1 mM), and GLi (10 μM) on EEJ induced relaxation in the endothelium-intact aorta rings precontracted with PE (10 μM). ^** P < 0.01 compared 4-AP treating group with control group;⁺⁺ P < 0.01 compared TEA treating group with control group;^## P < 0.01 compared BaCl₂ treating group with control group. (d) Effects of EEJ (1 g/L) on the cumulative concentration response for CaCl₂ (0.5 mM–8 mM) in high K⁺ (60 mM)-Ca²⁺-free depolarizing solution. ^** P < 0.01 compared with control group. (e) Effect of EEJ (1 g/L) on the PE (10 μM) precontracted endothelium-denuded aortic rings in the Ca²⁺-free K-H solution. ^** P < 0.01 compared with the Ca²⁺-containing group. (f) Influence of EEJ (1 g/L, 2 g/L) on the increase of [Ca²⁺]_i in ASMCs induced by KCl (30 mM). Verapamil (VER, 10 μM) was applied as the positive inhibition control group. ^** P < 0.01 EEJ (1 g/L) treating group compared with the control group; ^## P < 0.01 EEJ (2 g/L) treating group compared with the control group; ⁺⁺ P < 0.01 verapamil treating group compared with the control group.