Figure 2.

Original records showing the relaxations induced by (a) acetylcholine (ACh, 1 nM – 3 μM, as shown by downward arrows) and (b) 10 mM K⁺ (KCl) in tissues treated with high-K⁺ (60 mM) physiological salt solution (PSS), the Na⁺/K⁺-ATPase inhibitor ouabain (10 μM), the inward rectifier K⁺ channel inhibitor Ba²⁺ (50 μM), the gap junction inhibitor 18α-glycyrrhetinic acid (18α-GA, 50 μM), or the large-conductance Ca²⁺-activated K⁺ channel inhibitor charybdotoxin (100 nM) plus the small-conductance Ca²⁺-activated K⁺ channel inhibitor apamin (1 μM) (ChTX+apamin). All experiments were in the presence of L-NAME (100 μM). The first trace in the lower panel shows that 10 mM K⁺-induced relaxations could not be mimicked by equal molar NaCl. (▴) precontractions produced by 1 μM phenylephrine; (Δ) precontraction produced by high-K⁺ PSS.