Fig. 7. (  A ) Effect of protein kinase C inhibition (bisindolylmaleimide I [BIS1; 3 × 10⁻⁶m]), alone and in combination with ketamine, on acetylcholine (ACh)–induced increases in tension in endothelium-denuded pulmonary vein strips. (  B ) Effect of BIS1, alone and in combination with ketamine, on intracellular Ca²⁺concentration ([Ca²⁺]ⁱ) in acetylcholine-pretreated endothelium-denuded pulmonary vein strips. (  C ) Effect of BIS1, alone and in combination with ketamine, on the pulmonary vein [Ca²⁺]ⁱ–tension relation in acetylcholine-pretreated strips. BIS1 decreased acetylcholine-induced increases in tension (  P < 0.001), had no effect on [Ca²⁺]ⁱ(  P = 0.193), and caused a rightward shift (  P < 0.001) in the [Ca²⁺]ⁱ–tension relation. In the presence of BIS1, the ketamine-induced attenuation of the acetylcholine-induced increases in tension is abolished (  P = 0.607), with no effect on [Ca²⁺]ⁱ(  P = 0.193). Therefore, protein kinase C inhibition abolished (  P = 0.798) the ketamine-induced change in the [Ca²⁺]ⁱ–tension relation in acetylcholine-pretreated pulmonary vein strips. n = 6.