Yoshida, M. and Koeda, T. Effect of aminoglycoside antibiotics on the electrical stimula-tion-induced contractile response of the guinea-pig ureter. Japanese Tournal of Smooth Muscle Research., 1989, 25 (3), 75-87, 1989 Using electrical stimulation, we first inves-tigated whether the movement of ureteral smooth muscle of the guinea-pig was myogenic in its control, or neurogenic. We then investigated the effects of aminoglycoside antibiotics (kanamycin, bekanamycin and ribostamycin) on the movement of ureteral smooth muscle induced by electrical stimulation. In these investigations, each ureter removed from the animal was cut into three approximately equal-sized segments, which are an upper segment (kidney side), a middle segment and a lower segment (urinary bladder side). Each segment was mounted in an organ bath filled with Krebs solution and the mechanical response induced by electrical stimulation of each segment was recorded isometrically. Each one of the upper, the middle and the lower segments was stimulated with rectangular pulses (50 volt, 0.1-3 msec durations, 40 Hz) for a period of 2 sec. Of all segments tested (ten in each group), none showed any response to the stimulation with pulses below 0.5 msec duration. While 2-3 segments out of ten of the upper, the middle and the lower ureteral segments showed a contractile response to stimulation with pulses of 1 msec duration, the rest of the segments showed no response to the same stimulation. This contractile response was not inhibited by tetrodotoxin which is known to block the nerve-mediated response. And also, all the ten samples of each upper, middle and lower segment never failed to show a contractile response to stimulation with pulses of 2 msec and 3 msec duration. Various drugs which are already known to block the nerve-mediated response (i.e., atropine, guane-thidine, phentolamine, propranolol and tetrodotoxin) were tried, but none of them had an inhibitory effect on the contractile response. On the other hand, each one of kanamycin (KM), bekanamycin (AKM) and ribostamycin (RSM) in concentrations of 1×10^-5 g/ml-1×10^-3 g/ml produced a concentration-dependent decreasing effect in the magnitude of the electrical stimulation-induced contractile response of the ureteral segment. In addition, the decreasing effects of these antibiotics were also observed in the tetrodotoxin. From these results, we concluded that the contractile response of the ureter may be myogenic in its control, and the aminoglycoside antibiotics, KM, AKM and RSM, may act directly on the ureteral smooth muscle so as to decrease its contractile response.

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Ohkawa, H. Effects of calcitonin gene-related peptide on the non-adrenergic inhibitory potentials in the intestimal smooth muscle cells of the guinea pig. Japanese Tournal of Smooth Muscle Research, 25 (3), 98-96, 1989-Effects of calcitonin gene-related peptide (CGRP) on the spontaneous and evoked contractions in the duodenal and ileal preparations, the spontaneous action potentials and the non-adrenergic non-cholinergic inhibitory poten-tials (NANC i.p.s) in the longitudinal smooth muscle cells of the guinea-pig duodenum and ileum were examined. Preparations were pretreated with atropine (1 μM) and guanethidine (5 μM). CGRP (26 nM) was found to inhibit spontaneous and evoked contractions. The resting membrane potential of the longitudinal smooth muscle was not altered but the frquency of spontaneous action potentials was decreased by the treatment with CGRP (6-104 nM). Field stimulation evoked the NANC i.p.s and the pretreatment with atropine (1 μM) and guanethidine (5 μM) caused an increase in the amplitude of the NANC i.p.s in the longitudinal smooth muscle. However, CGRP (6-104 nM) did not change the amplitude of the NANC i.p.s. The rebound excitation in the longitudinal muscle membrane was inhib-ited by CGRP. The single spike activity of the myenteric neurons in the duodenum was not affected by CGRP (26-104 nM). The results suggest that CGRP inhibits the intestinal motility by non-neurogenic NANC manner and does not activate the NANC inhibitory neurons in intestine.

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Interdigestive motor complex (IMC) from the stomach to the ileum and colonic migrating motor complex (CMMC), and the effects of motilin and PYY to them were studied in conscious dogs with strain gauge force transducers (SG).
In fasted dogs, IMC cycle times were 100.5±7.5 min in from the antrum to the ileum and propagation velocity of the small intestine was fastest in the proximal jejunum (4.85±0.81 cm/min), slowest in the distal ileum (0.81±0.08 cm/min). The duration of postprandial interruption of motor complex (DIMC) was longer in the antrum and duodenum in 8 dogs of the twelves than the middle and lower intestines.
Ileo-colonic propagation rates of IMC that reached to the terminal ileum were 95/116 (81.9%), but the frequency of CMMCs was about 4 times higher than that of MCs.
Each colonic motor complex were classified into four patterns, such as aboral migrating complex (A), oral migrating complex (O), discrete complex (D) and giant migrating contractions (G), and the starting point of migrating complex was marked with^-, like A, O or G. Thus, independency index (I I) in each site was defined as: II= (sum of number of A, O, G and D) / (total number of colonic motor complex). II was highest in colon 1 (70-80%) and next in colon 4.
Motilin (0.5μg/kg·hr) elicited IMC like activities in the antrum, duodenum andproximal jejunum, but no effects in the middle and lower small intestine, and the colon. PYY infusion caused dose dependent inhibitions of IMC in the antrum and duodenum, but no effects in the below intestines as same as motilin. These findings suggest that IMCs are basal rhythms of gastrointestinal motility and IMCs occurring from the antrum to the proximal jejunum are more sensitive to the factors as eating or gut peptides.

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The mechanism of the occurence of anti-peristaltic discharge originated in the stomach distal to the transection followed by end-to-end anastomosis has not been elucidated.
The purpose of this study is to investigate the effect of the enteric nervous system on the anti-peristaltic discharge in the canine stomach distal to the transection by using sodium channel blocking agent TTX and ganglion blocking agent C₆ together with local anesthetic lidocaine electromyographycally.
Following results were obtained.
1. The retardation of propagation velocity of normo-peristaltic discharge and the decrease of frequency of anti-peristaltic discharge were noted both at TTX 10μg/kg iv. and TTX 10μg/kg iv. together with mucosal anesthetization by lidocaine. And no significant difference was recognized between them.
2. The retardation of propagation velocity of normo-peristaltic discharge and the decrease of frequency of anti-peristaltic discharge were noted at C₆ 10 mg/kg iv. together with mucosal anesthetization by lidocaine. While the decrease of frequency of anti-peris-taltic discharge was only noted at C₆ 10 mg/kg iv.,
Conclusively, it was suggested that the nervous pathway which transmits some excitive information from mucosa to the myenteric plexus exists and that the myenteric plexus has a important role on the occurence of anti-peristaltic discharge.

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