Effects of Vc1.1 and cVc1.1 on pseudo‐related pain responses to colorectal distension in healthy and CVH mice. (A) In healthy mice, VMR to colorectal distension (CRD) were not significantly changed by intra‐colonic administration of linear Vc1.1 (1 μM), relative to administration of vehicle. Vehicle: N = 10 mice; Vc1.1: N = 6 mice. Data shown are AUC of the corresponding EMG signal (means ± SEM). (B) In CVH mice, intra‐colonic administration of linear Vc1.1 (1 μM) significantly inhibited the VMR to CRD, particularly at distension pressures of 40 mmHg and 60 mmHg. Vehicle: N = 10 mice, Vc1.1: N = 7 mice. *P < 0.05; significantly different from vehicle; generalized estimating equations test followed by LSD post hoc test. (C) Intra‐colonic administration of cVc1.1 (1 μM) did not affect VMRs to CRD in healthy mice relative to vehicle treated mice. Vehicle: N = 8 mice, cVc1.1: N = 7 mice. (D) In CVH mice, intra‐colonic administration of cVc1.1 significantly reduced VMRs to colorectal distension, particularly at distension pressures of 40 mmHg, 60 mmHg and 80 mmHg. Vehicle: N = 10 mice, cVc1.1: N = 8 mice. *P < 0.05, significantly different from vehicle; generalized estimating equations test followed by LSD post hoc test. (E) Representative tracing of the raw abdominal EMG signals assessing the VMR to 60 mmHg (20 s duration, indicated by horizontal bar) of CRD in healthy control (HC) mice after (E, panel i) vehicle or (E, panel ii) cVc1.1 and in mice with CVH after (E, panel iii) vehicle or (E, panel iv) cVc1.1. Length of recording shown 45 s. (F) Colonic compliance in both healthy and CVH mice was not altered by intra‐colonic cVc1.1 (1 μM) administration, compared with intra‐colonic administration of vehicle. Data were statistically analysed by generalized estimating equations followed by the LSD post hoc test.