Mechanisms mediating CCK-8S-induced contraction of proximal colon in guinea pigs

Figure 1 Effects of CCK-8S on the resting tension of guinea pig proximal colonic smooth muscle (PCSM) strips. A: Representative traces of the effect of CCK-8S (10^-7 mol/L) on the resting tension of circular muscle (CM) strips. CCK-8S increased the mean contractile amplitude of CM strips, which was inhibited by pretreatment with CCK1 receptor antagonist devazepide (10^-7 mol/L), L-type calcium channel inhibitor nifedipine (10^-5 mol/L), Ca²⁺-ATPase inhibitor thapsigargin (TG) (10^-5 mol/L) and intracellular calcium chelator BAPTA-AM (BA) (10^-5 mol/L). Pretreating CM strips with iberiotoxin (10^-6 mol/L), a selective potassium channel inhibitor, did not block the CCK-8S-induced increase in the contractile amplitude of CM strips but decreased the frequency; B: Representative traces of the effect of CCK-8S (10^-7 mol/L) on the resting tension of longitudinal muscle (LM) strips. The CCK-8S-induced increase in the amplitude and frequency of LM strips was inhibited by pretreatment with devazepide (10^-7 mol/L), nifedipine (10^-5 mol/L) or TG (10^-5 mol/L) and BA (10^-5 mol/L). Pretreating LM strips with iberiotoxin (10^-6 mol/L) did not attenuate the CCK-8S-induced increase in the contractile amplitude of LM strips but decreased the frequency. CCK2 receptor antagonist CI 988 had no effect on the CCK-8S-induced contraction of CM and LM strips.