Effect of cisapride on the cholinergic control mechanisms of gastrointestinal motility in dogs.

Fujii, Kohyu; Okajima, Masazumi; Kawahori, Katsufumi

doi:10.1540/jsmr1965.24.1

Cited by 13 publications

(9 citation statements)

References 8 publications

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“…Therefore, these medicines have been known to cause a great deal of pain when administered to thoroughbreds with hypersensitive sensory nerves [9]. Recently, cisapride was developed as a motility enhancing drug for the entire digestive tract, and as a medicine without a 5-HT 4 antagonist [12]. Moreover, it is known that cisapride has a regulatory action on gastrointestinal motility to promote the release of acetylcholine, and to promote as effectively as motilin, through the serotonin receptor (5-HT 4 ), which exists in the digestive tract's myenteric plexus [12,62,67].…”

Section: The Gastrointestinal Prokinetic Agent (Serotonin Receptor Agmentioning

confidence: 99%

“…Recently, cisapride was developed as a motility enhancing drug for the entire digestive tract, and as a medicine without a 5-HT 4 antagonist [12]. Moreover, it is known that cisapride has a regulatory action on gastrointestinal motility to promote the release of acetylcholine, and to promote as effectively as motilin, through the serotonin receptor (5-HT 4 ), which exists in the digestive tract's myenteric plexus [12,62,67]. In horses, cisapride has been mainly given orally [9] to treat flatulence or constipation colic or to prevent postoperative ileus [15,34,70].…”

Section: The Gastrointestinal Prokinetic Agent (Serotonin Receptor Agmentioning

confidence: 99%

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Medicinal Treatment to Equine Gastrointestinal Dysfunctions

Sasaki

Yamada

Hara

2003

JES

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This study was designed to investigate gastrointestinal dysfunctions, especially the effects of gastrointestinal prokinetic agents on digestive disorders involving lowered motility. The effects of α 2-adrenergic agonists for treating acute abdominal disorders involving intestinal torsion in horses were also investigated. The results are as follows: (1) It appeared that the functions of migrating contractions (MC) in horses were to transfer the contents of the digestive tract as soon as possible to the cecum and colon, in addition to maintaining homeostatis in the digestive tract. (2) Motilin was seen to be involved in the regulation mechanism of intestinal motility in the horse as well as in humans and dogs, and brought about MC. (3) The intravenous injection of cisapride brought about MC in the small intestine. With administration of a higher dose of 0.75 or 1.0 mg/kg, a significant increase (P<0.05) in MC frequency was observed. (4) It was clear that the inhibitory effects of the α 2adrenergic agonists persisted for a longer time with a more remarkable reduction of contractions in the cecum and colon than in the jejunum. When α 2-adrenergic agonists are used for relieving intestinal tension, it is recommended that medetomidine is more effective than xylazine.

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Section: The Gastrointestinal Prokinetic Agent (Serotonin Receptor Agmentioning

confidence: 99%

Section: The Gastrointestinal Prokinetic Agent (Serotonin Receptor Agmentioning

confidence: 99%

Medicinal Treatment to Equine Gastrointestinal Dysfunctions

Sasaki

Yamada

Hara

2003

JES

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“…There is evidence to suggest that the substituted benzamide cisapride, which has prokinetic properties and stimulates the phasic motor activity of the gastrointestinal tract by potentiating the release of acetylcholine from postganglionic cholinergic nerves (Chey et al ., 1984; Suzuki et al ., 1985; Schemann & Ehrlein, 1986; Fujii et al ., 1988; Strombeck et al ., 1988; Schuurkes & Van Nueten, 1990), may also promote detrusor muscle motility. This action appears to be beneficial in cases of urinary retention caused by several agents and clinical studies have reported successful use of cisapride in the treatment of neuropathic bladder (Ettienne et al ., 1988), in urinary retention following prostatechtomy (Meier et al ., 1996), or even in cases of lazy bladder syndrome (Franceschetti et al ., 1997; Kroll et al ., 1998).…”

Section: Introductionmentioning

confidence: 99%

Cisapride reverses the anticholinergic effect of disopyramide on the isolated guinea‐pig urinary bladder

Koutsoviti-Papadopoulou

Nikolaidis

Batzias

et al. 2002

Vet Pharm & Therapeutics

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The present investigation aims to examine whether the prokinetic agent cisapride is able to reverse disopyramide's anticholinergic effect on the isolated guinea-pig urinary bladder. Acetylcholine, at concentrations ranging from 10(-7) to 10(-3) M, produced a stimulatory effect on the urinary bladder (pEC(50) value=5.1). Disopyramide competitively antagonized the contractile effect of acetylcholine with an ID(50)=4.4 x 10(-6) M. Although cisapride by itself had either no intrinsic contractile action or a modest effect on the urinary bladder, at concentrations ranging from 3 x 10(-7) to 10(-6) M, it significantly reversed the above inhibitory effect of disopyramide, and produced a parallel leftward shift of the concentration-response curve for acetylcholine in the presence of disopyramide. The pEC(50) values for acetylcholine in the presence of 3 x 10(-6) M and 10(-5) M disopyramide were 4.7 and 4.2, respectively, while in the presence of 10(-5) M disopyramide, after pretreatment with 5 x 10(-7) M cisapride, the pEC(50) value for acetylcholine was 4.6. It is concluded that cisapride is effective in reversing the anticholinergic activity of disopyramide on the isolated guinea-pig urinary bladder, probably by facilitating cholinergic neurotransmission.

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“…To clarify whether glucagon inhibited antral motility or not, I investigated the effects of glucagon on contractions induced by cisapride, which is known to be an agonist at neural 5-hydroxytryptamine (5-HT) 4 receptors in the cholinergic motor path- ways and accelerates endogenous acetylcholine release from cholinergic nerve endings in the myenteric plexus (Hardcastle et al, 1984 ;Suzuki et al, 1985 ;Fujii et al, 1988 ;Taniyama et al, 1991). Cisapride induced strong rhythmical contractions in every region (Fig .…”

Section: Discussionmentioning

confidence: 99%

Involvement of Cholinergic Motor Neurons in Pharmacological Regulation of Gastrointestinal Motility by Glucagon in Conscious Dogs.

Shimatani

1997

J. Smooth Muscle Res.

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To clarify the exact mechanisms of the pharmacological effects of glucagon on gastro intestinal motility, the following experiments were performed on the conscious and anesthe tized dogs. 1) During phase I of interdigestive migrating contractions (IMC) , glucagon (5 infusion for 5 minutes) induced phasic contractions in the duodenum , jejunum and ileum, but not in the antrum. These excitatory responses were also observed in the truncal vagotomized dogs. These contractions were abolished by atropine or hex amethonium in the conscious dogs, and also by tetrodotoxin in the anesthetized dogs . 2) Glucagon inhibited cisapride-induced contractions only in the antrum in the conscious dogs .After pre-treatment with hexamethonium, glucagon inhibited these contractions in the duodenum, jejunum and ileum as well as in the antrum. After pre-treatment with tetrodotoxin in the anesthetized dogs, glucagon did not affect acetylcholine-induced contrac tions in any region. 3) Glucagon inhibited spontaneous phase III contractions and eryth romycin-induced phase III-like contractions in the antrum, but did not inhibit either contrac tions in the other regions in the conscious dogs. These paradoxical effects of glucagon between the antrum and intestine were similar to those involved in the blockade of 5-hydroxytryptamine 3 receptors. After pre-treatment with hexamethonium , glucagon inhib ited these contractions in the duodenum, jejunum and ileum as well as in the antrum . In conclusion: 1) Glucagon latently inhibits cholinergic motor activities in the antrum and intestine not directly, by binding to either receptor on the smooth muscle cells , but through postganglionic cholinergic neurons and possibly through 5-hydroxytryptamine neurons. 2) On the other hand, in the intestine the reverse effects through preganglionic cholinergic neurons involving nicotinic and muscarinic receptors are more potent . 3) As a result, glucagon inhibits antral contractions and does not affect intestinal contractions in a con scious state.

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Effect of cisapride on the cholinergic control mechanisms of gastrointestinal motility in dogs.

Cited by 13 publications

References 8 publications

Medicinal Treatment to Equine Gastrointestinal Dysfunctions

Medicinal Treatment to Equine Gastrointestinal Dysfunctions

Cisapride reverses the anticholinergic effect of disopyramide on the isolated guinea‐pig urinary bladder

Involvement of Cholinergic Motor Neurons in Pharmacological Regulation of Gastrointestinal Motility by Glucagon in Conscious Dogs.

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