An effect of caerulein was studied on a contractile response of the ileal longitudinal smooth muscle isolated from seven animal species, monkey, dog, rabbit, guinea-pig, rat, vole and mouse. In isotonic recording, caerulein induced a contraction in the muscle isolated from all animal species . Sensitivities of ileal strips to caerulein in the contractile response was divided into three groups. That is, a high sensitive group; dog and guinea-pig, a middle sensitive group; rabbit and vole, a low sensitive group; monkey, rat and mouse. In another series of experiment, effect of several antagonists was examined on the caerulein-induced contraction in ileal muscle of dog, rabbit or guinea-pig. TTX inhibited the contractions in all the ilea. As the contraction was inhibited by atropine and scopolamine in dog ileum but not in rabbit one, the contraction may be due to an excitation of the cholinergic neuron or an excitation of non-cholinergic excitatory neuron, respectively. On the other hand, it is supposed that the contraction in guinea-pig ileum is involved to both the neurons because the contraction was inhibited partially by scopolamine and not by atropine . In conclusion, the ilea isolated from seven animal species showed species differences in sensitivity to caerulein in contractile response, and caerulein seems induces the contractions involving to different nervous systems in dog, rabbit or guinea-pig ileum, respectively.

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Correlation of intestinal motility and serum motilin after abdominal surgery was investigated experimentally and clinically. The results were summarized as follows:
1) The recovery of intestinal motility was faster in the dogs simply laparotomized than gastrectomized.
2) The recovery of the small intestinal motility was followed by that of the large intestinal motility in the dogs.
3) The intravenous infusion of the synthetic motilin markedly stimulated the intestinal motor activity in early postoperative period.
4) Serum motilin levels significantly dropped once after abdominal surgery and rose again both in the dogs and the patients.
5) The rate of increase of serum motilin levels at the postoperative period closely correlated with the recovery of the intestinal motility both in the dogs and the patients, that is, the higher the rate of increase was, the faster the recovery was.

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The urethral pressure profile (UPP) was studied and compared in anesthetized and decerebrated dogs. The maximum urethral closure pressure (UPmax) was measured in various procedures.
In anesthetized dogs UPmax was 70.9±22.9cmH₂O (mean±S.D.) in control, 40.2±16.4cmH₂O in laparotomy and 26.5±12.5cmH₂O in resection of pubic bone.
As procedures were added, UPmax decreased, and the shape of UPP in anesthetized dogs showed remarkable change. In decerebrated dogs UPmax was 96.9±14.9cmH₂O in control, 77.5±28.0cmH₂O in decerebration, 78.1±7.0cmH₂O in 3hours after decerebration, 79.0±6.8cmH₂O in laparotomy and 49.6±7.0cmH₂O in resection of pubic bone. UPP in decerebrated dogs generally kept its shape in various procedures and UPmax showed no change before and after laparotomy.
Therefore, decerebrated dogs were considered to be useful for the experimental model of UPP.

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Effects of electrical stimulation of the inciser tooth pulp on the gastrointestinal motility were investigated in the rabbit anesthetized with urethane and chloralose.
1. Pulpal Stimulation caused an excitatory or an inhibitory effect in the gastric body and antrum and the ducodenum. After bilateral splanchnicotomy the excitatory response to the pulpal stimuation was reinforced or the inhibitory response converted to the excitatory response. An additional cervical vagotomy abolished the excitatory and inhibitory response.
2. Atropine diminished the spontaneous efferent discharges of vagal gastric branch (VGB) and abolished the excitatory and inhibitory response to stimulation of the pulp and the inferior alveolar nerve. This agent also blocked the potentials of the VGB evoked by afferent stimulation of the inferior aveolar nerve.
3. Hexamethonium bromide abolished the excitatory and inhibitory responses to the pulpal stimulation but did not affect spontaneous discharges and increased discharges of the VGB to pulpal stimulation.
4. Morphine produced decreased rate of the spontaneous discharge of the VGB and abolished increased rate of discharges of the VGB as well as the gastrointestinal responses to pulpal stimulation.
5. It is concluded from these results that the afferent impulses caused by pulpal stimulation and the inferior alveolar nerve‘'reflexly’ activate the vagal moter nuclei in the medulla oblongata and the sympathetic splanchnic nuclei in the thoracic segments through the trigeminal nerve: The vagus nerves produced the excitatory response in the gastrointestinal motility, while the splanchnic nerves caused the inhibitory response.
6. It was supposed that sites of action of atropine and morphine is not in peripheral site, but in the central nerves site.

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The histamine-induced contractions and effects of some smooth muscle relaxants on their contractions were examined in the guinea-pig taenia coli. Application of Ca to the Ca-free physiological solution caused a contraction of the taenia coli (Ca contration), and histamine accelerated and increased the Ca contraction (H · Ca contraction). Histamine also contracted the taenia coli in the Ca-free solution (Ca (-) · H contraction). D-600 which preferentially reduces the Ca influx into muscle cells, more effectively depressed the H · Ca contraction and more feebly the Ca (-) · H contraction than histamine-induced contraction in the normal physiological solution. Papaverine inhibited the H · Ca contraction and the Ca (-) · H contraction more than the histamine-induced contration. Benactyzine was a specific agent against the Ca (-) · H contraction.
When the Ca contraction reached the peak, application of histamine induced a further contraction. D-600 effectively inhibited the Ca contraction and the further contraction induced by histamine. Although papaverine blocked the Ca contraction similamly to D-600, the application of histamine produced a large contraction. Benactyzine induced only a feeble inhibition on the Ca contraction, but it was effective against the following contraction caused by histamine.
Histamine probably mobilizes the extracellular and cellular Ca and contracts the smooth muscle. Papaverine seemn to ishibit smooth muscle contractions by diverse actions. Benactyzine may exert the main inhibtion on the mobilization of the cellular Ca through the competition with Ca. In the intestinal smooth muscle, nitroprusside which is known to act on intracellular binding sites for Ca in some vascular smooth muscle is entirely different from benactyzine.

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In the guinea-pig ileal Longitudinal smooth muscle, Ba caused an initial phasic contraction, followed by a gradual decrease of the contraction (tonic contraction). In the Ca-free and the Ca-free, K-rich physiological solution, Ba could also contract the longitudinal muscle, but 30min- and 60min-immersion of the tissue in the Ca-free solution decreased lower than 20% of control of the Ba contraction. Although the Kinduced depolarization intensified the Ba contraction after the 30min-immersion, within 10min after the immersion in the two solutions there is no difference in the height of Ba contractions. In the normal physiological solution, Ba seems to serve the contractile protein with free Ca ions rather than itself for the Ba contraction. D-600 induced an equal inhibition on the Ba contractions in the normal physiological solution and in the Ca-free solution, and it inhibited the tonic contraction more than the phasic one. The phasic component may be due to the cellular Ca mobilized by Ba which passes through D-600-sensitive pathway, and at least part of the tonic component may utilize the extracellular Ca. Bencetyzine perferentially inhibited the Ba contraction in the Ca-free solution, and it depressed the phasic component more than the tonic one. Treatment with papaverine induced an equal inhibition on the phasic and tonic components of Ba contractions and the Ba contraction in the Ca-free solution .Benactyzine may exert the main influence on the mobilization of the cellular Ca through the competition with Ca. Papaverine seems to inhibit the Ba contractions by diverse actions.

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Effects of some α- and β-adrenoceptor agonists were investigated on the isolated rabbit sphincter of Oddi and duodenum.
1. In both preparations, noradrenaline (10^-6-10^-5M) inhibited the rhythmic spontaneous contractions, and the inhibition was observed more markedly in the sphincter than in the duodenum.
2. In the duodenum, phenylephrine (10^-6-10^-5M) induced an inhibition of the contractions of rapid onset followed by an increase in contraction height. The response resembled that by noradrenaline in the presence of propranolol 10^-6M. 10^-5M of phenylephrine introduced the increase in contractions more remarkably than 10^-6 M of the drug. Isoproterenol (10^-7-10^-6M), as well as noradrenaline in the presence of phentolamine 10^-5M, proudced an inhibition of slow onset which was maintained throughout the presence of the drug. The inhibition by noradrenaline with phentolamine was more intense than that without phentolamine. Qualitatively similar responses to phenylephrine and isoproterenol were observed on the sphincter of Oddi.
3. In both preparations, tetrodotoxin at 10^-7M potentiated the inhibition induced by noradrenaline, depressed the increase in contractions by phenylephrine, but hardly affected the response to isoproterenol.
4. The results indicate that, in the sphincter of Oddi and duodenum in rabbits, adrenergic agonists produce inhibition of the contractions via α- and β-receptors in the smooth muscle fibres, and abrupt inhibition by α-agonist may cause excitatory response mediated through neural consequence.

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Many workers have reported that α-adrenergic drugs activate and β-adrenergic drugs suppress the ureteral activity. On the other hand, recent studies have proved that the pacemaker in the renal pelvis controles the ureteral peristalsis .
In this study, in vivo and in vitro experiments were performed to explore the effects of autonomic drugs on pelvic pacemaker controling the ureteral peristalsis .
It was suggested that both of noradrenaline and isoproterenol stimulated the pacemaker activity itself, the former, however, elevated the renal pelvic pressure to accelerate the propagation of pacemaker activity consequentry, while the latter decreased the renal pelvic pressure to suppress the propagation consequently .Acetylcholine stimulated the pacemaker activity and its propagation transiently, but base line of renal pelvic pressure with increased contraction pressure was decreased after drug administration. Furthermore, acetylcholine sometimes developed the retrograde peristaltic contraction from ureter to pacemaker region through the pelviureteral junction. Then acetylcholine might affect directly on ureter rather than on pacemaker itself and its propagation.

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