ABSTRACT
Objective To investigate the effect of cholecystokinin (CCK) on colon motility and its mechanism in development of irritable bowel syndrome via recording ionic channels currents and contraction of guinea-pig proximal colon. Methods The guinea-pigs (body weight ranged from 200 g to 250 g) were deprived of food, but not water, for 12 hours before experiment. The animal was sacrificed and 6 cm of proximal colon was obtained. The contractile activity of isolated proximal colon in 1 × 10-7 ,5 × 10-7 or 1 × 10-6 mol/L of CCK-8 solution was recorded. The impact of 1 × 10-7 , 5 × 10-7 and 1 × 10-6 mol/L of CCK-8 and 1 × 10-6 mol/L CCK-8 nifidipin on current of calcium activated potassium channel (IBKac) was detected with an EPC-10 amplifier and an image analysis software.Results In comparison with blank [(0. 68 ±0. 12) g], the amplitude of colon contraction in 1 × 10-7 ,5×10-7 and 1×10-6 mol/L of CCK-8 was increased by (15. 0±1.5)%,(28. 0±1.4)%, and (36.0±1.6) %, respectively ( n = 7, P = 0. 023,0. 005 and 0. 01 ), but there was no significant change of frequency. When exogenous stimulation at +60 mV, the current of IBKac was enhanced to (117. 45 ± 3.60)%, (125.42± 5. 30)% or (136. 98±6. 80)% in 10-7 ,5 × 10-7 or 10-6 mol/L of CCK-8,respectively, compared with controls (n= 7, P＜0.01 ). However, after adding nifidipin, the current of IBKca was reduced to (102.23±5.60)% in 10-6mol/L of CCK-8 at +60 mV when compared with controls (n=7, P= 1. 491 ). Conclusion CCK enhances proximal colonic motility by increasing Ca2+ influx and IBKac current, which is characterized by enhancement of amplitude of contraction.