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World J Gastroenterol. Mar 7, 2010; 16(9): 1076-1085
Published online Mar 7, 2010. doi: 10.3748/wjg.v16.i9.1076
Published online Mar 7, 2010. doi: 10.3748/wjg.v16.i9.1076
Figure 3 Effects of CCK-8S on AP of PCSMCs.
A-C and E: CCK-8S (10-7 mol/L) suppressed the amplitude of AP to 38.6% ± 3.2% (n = 15, P < 0.01); A, B, D and F: CCK-8S (10-7 mol/L) decreased fast repolarization times (T90) by 36.9% ± 8.7% (n = 15, P < 0.01); A and E: Nifedipine (10-5 mol/L) blocked the effects of CCK-8S on the amplitude of AP but failed to have any effect on T90; B and F: Iberiotoxin (10-6 mol/L) blocked the effects of CCK-8S on T90 but failed to have any effect on the amplitude of AP; E and F: Pretreating SMCs with devazepide (10-7 mol/L) blocked the CCK-8S-evoked effect on AP amplitude and T90, whereas CI 988 had no such effect. aP < 0.01 vs control group (CaPSS); bP < 0.01 vs CCK-8S group; cP > 0.05 vs control group.
- Citation: Zhu J, Chen L, Xia H, Luo HS. Mechanisms mediating CCK-8S-induced contraction of proximal colon in guinea pigs. World J Gastroenterol 2010; 16(9): 1076-1085
- URL: https://www.wjgnet.com/1007-9327/full/v16/i9/1076.htm
- DOI: https://dx.doi.org/10.3748/wjg.v16.i9.1076