The following results were obtained from investigations of the mechanisms of propagation of the interdigestive migrating electric complex (IMEC) obtained by inducing action potential from dogs in a fasted conscious state according to anastomosis of the transected small intestine.
1. The IMEC occuring on the oral side always showed normal cotinuous propagation in the stump of the blind loop with no anastomosis in the small intestine.
2. Even in cases of transplantation of the small intestine in different parts of the same digestive tract during IMEC propagation, the IMEC skipped over this and propagation showed normal continuity.
3. From the above results, it appears that the normal mechanism of propagation occurs with no relation to anastomosis of the small intestine, and movement of the intestinal contents also play no role. It is therefore assumed that coordination of the propagation of IMEC is via the exrinsic nervous system.
4. When the distal small intestine was transected, the frequency of the IMEC was the same as the frequency of the distal BER and the velocity was also decreased. The transplanted samll intestine maintained the normal propagation velocity after transection. New electric complexes were seen from the stump of the distal intestine and they migrated to the caudal side.
From these results, it appears that the propagation of IMEC also occurs via nervous systems other than the extrinsic nervous system and that innervation by regulation of the extrinsic and intrinsic nervous system is involved in the propagation of IMEC.

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The calmodulin levels of human and rat myometrium were measured during pregnancy and under estrogen, progesterone administration, and uterine muscle contraction at the same time was also measured. The calmodulin concentration in the uterine muscle was increased as the stage of pregnancy advanced. This increase also intensified. the maximum contractility of the uterine muscle together with the increase of growth during pregnancy. The calmodulin levels were increased by the administration of estrogen and this increase was restricted by progesterone. As a result, the adjustment of the calmodulin level by administration of these steroid hormones was found to be a very interesting mechanism for studying the physiology of uterine muscle contractions.

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Sunano, S., Shimada, T. and Shimamura, K. Effects of sodium vanadate on the smooth muscle of the guinea-pig was deferens. Japanese Journal of Smooth Muscle Research, 1985, 21 (2), 95-105.- Effects of sodium vanadate on electrical and mechanical activities of smooth muscle of the guinea-pig was deferens were investigated. Sodium vanadate of concentrations higher than 5×10^-6M caused an elevation of basal tension and, at concentrations higher than 5×10^-4M, initiated spontaneous contractions. These effects were not blocked by treatments with reserpine, tetrodotoxin or phentolamine. Treatment with ouabain also did not block the tension development by sodium vanadate. Sodium vanadate caused slight depolarization of membrane and potentiated spike activities. The phasic contraction of potassium contracture was potentiated by sodium vanadate in a similar manner to pretreatment with 15 mM K⁺ or with ouabain, both treatments occasioning slight depolarization. Sodium vanadate also caused tension development in K-depolarized preparetions. Contrastingly, drug-induced contractions were not significantly affected by sodium vanadate.
It is suggested that sodium vanadate acts directly on smooth muscles and causes tension development without relation to Na, K-ATPase activity. Changes in the membrane electrical activities may be part of the cause of contraction. However, it can also initiate tension development without membrane potential changes, presumably acting on intracellular Ca binding sites.

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Abstract Shimada, T. and Sunano, S. Contraction independent of extracellular Ca by sodium vanadate in guinea-pig vas deferens. Japanese Journal of Smooth Muscle Reserach, 1985, 21 (2), 107-117.-The effects of Ca removal and Ca antagonists on sodium vanadate-induced contractions of the guinea-pig vas deferens were studied. Sodium vanadate-induced tension development could be observed even 120 minutes after the removal of Ca, whereas K-contracture disappeared within 20 minutes. Spontaneous contractions induced by sodium vanadate were abolished by the removal of Ca. Verapamil and nifedipine did not show any effect on sodium vanadate-induced contraction, contrastingly, they blocked spontaneous contractions initiated by sodium vanadate. The effects of sodium vanadate on Ca contracture of depolarized prepara-tions were also studied. Though the drug potentiated phasic contraction, it did not potentiate tonic component of Ca contracture.
It was demonstrated that sodium vanadate induced tension development indepen-dently of extracellular Ca, presumably by releasing intracellularly bound Ca.

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I tried to make it clear three dimensional picture of the smooth muscle of the human gallbladder at first, and found a connection between the smooth muscle and the autonomic nerves in the wall.
At autopsy the gallbladder without lesion was collected from 15 males and 7 females died of apoplexy, head injury or myocardial infarction. These material wasfixed 10% neural formalin, impregnated into Masson Trichrome for smooth muscle, and modified Golgi method for nerve fivers, embeded in celloidin.
I laid a picture after another after tracing serial tangential section of 8μm by using camera lucida, and made three dimensional picture. In autonomic nerve in the wall three dimensional sections of 100-150μm were made and observed with light microscope.
Three dimensional muscle structure showed monounit structure, having meshwork structure from mucosal area to serous one. It was gratified the condition of the gallbladder contraction to illustrate a series of connection from mucosal aspect to serous one. Many fine nerve fivers were found forming plexuses in the subserouslayer, muscular layer and mucosa. There was close relationship between smooth muscle and intramural nerve fibers, which especially distributed into meshwork structure of muscle. I could find morphological relation among the layers, such as three main plexuses. It was suggested that subserous plexus had extrinsic nature.

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Cisapride strongly stimulates gastrointestinal motor activity simultaneously from stomach to jejunum in the interdigestive state. The contractile pattern in the stomach was quite similar to that of the natural interdigestive mingrating contractions (IMC) in all respects, frequecy, contractile force, and coordination between the gastric body and antrum. However, the cisapride-induced IMC-like contractions in the stomach did not migrate along the small intestine, nor were accompanied by an increase of plasma motilin concentration. Furthermore, both motilin and cisapride, given during the period of phase III, did not affect the phase III activity, but carbachol abruptly stopped phase III activity if it was given during phase TTI activity.
On the contrary, cisapride-induced contractions in the stomach are completely inhibited by atropine, pentagastrin, CCK-octapeptide, but not by secretin. These findings provide additional evidence to indicate that the cisapride-induced contractions in the stomach are identical with the natural IMC in the respect of reactons to hormonal substances. No noticeable side effects were observed.
In conclusion, cisapride is a unique compound to initiate IMC-like contractions in the stomach, but the contractions were not accompanied by an increase in plasma motilin concen-tration and did not migrate the small intestine.

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