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At least 865 records · Page 48Linked to original sources
PubMed1988

A comparative study of the effects of four choline esters on the secretion of fluid and glycoprotein from rat submandibular glands.

The actions of four choline esters, acetylcholine (ACH), methacholine (MET), carbachol (CAR) and bethanechol (BET), on the secretion of saliva and the specific glycoprotein (GP) contained in the secretory cells of the submandibular gland (SMG) of the rat were compared under conditions with and without physostigmine (PHY). The ED50 values with respect to salivation were 17 mg/kg for ACH, 1060 micrograms/kg for BET, 810 micrograms/kg for MET and 75 micrograms/kg for CAR, whereas after pretreatment with PHY, ED50 values were lowered to 7.5 mg/kg for ACH and 212 micrograms/kg for MET, but remained unchanged for CAR and BET. SDS-polyacrylamide gel electrophoresis demonstrated that the saliva from the SMG elicited by the four choline esters contained GP I (130 KDa) and GP IV (21.5 KDa), characteristic of the acinus, and a band of GP III (31 KDa), which originates from the granular tubules. The order of intensity of these bands was band I much greater than band III = band IV. Among these bands, band I increased in intensity in a dose-dependent manner. These results suggest that the four choline esters act mainly on the acinar cells, but exert some effects on the granular tubules of the rat SMG.

Acetylcholine↗
PubMed1989

Inhibitory effect of intravenous GABA antagonists on gastric acid secretion stimulated by secretagogues in rats.

Effect of intravenous administration of GABA antagonists on gastric acid secretion in perfused stomachs was studied in rats anesthetized with urethane. Bethanechol (BeCh)-stimulated acid secretion was definitely inhibited by bicuculline, a GABA antagonist, and strychnine, a glycine antagonist, but not by picrotoxin and pentylenetetrazol, GABA antagonists. The inhibitory effect of bicuculline and strychnine was accompanied by vigorous convulsions. Only the bicuculline-induced inhibition was still seen in d-tubocurarine paralyzed rats, and it was abolished in spinal rats. 2-Deoxy-D-glucose (2-DG)-stimulated acid secretion was apparently depressed by all the GABA antagonists of bicuculline, picrotoxin and pentylenetetrazol. The inhibitory effect of picrotoxin, but not bicuculline, on the 2-DG stimulation was still elicited in spinal rats. Inhibition of acid secretion stimulated by pentobarbital, a centrally acting secretagogue, was produced by picrotoxin and pentylenetetrazol in spinal rats. These findings suggest that bicuculline acts centrally to inhibit acid secretion stimulated both peripherally by BeCh and centrally by 2-DG, besides nonspecific mechanisms due to convulsions, and the action would be directed to centers which are implicated in stimulation of the sympatho-adrenomedullary system; picrotoxin and pentylenetetrazol also act centrally to inhibit 2-DG- or pentobarbital-stimulated acid secretion through depression of the central vagal tone which leads to inhibition of gastric acid secretion.

Animals↗
PubMed1990

Effects of GABA antagonists and structural GABA analogues on baclofen stimulated gastric acid secretion in the rat.

The effects of GABA receptor antagonists (bicuculline and phaclofen) and structural GABA-analogues on baclofen stimulated gastric acid secretion were studied in standardized perfused rat stomach preparations. Pretreatment with bicuculline, a GABAA-receptor antagonist, in the doses of 1 and 3 mg/kg, subcutaneously, had no influence on the gastric acid response to baclofen. In addition, phaclofen, a GABAB antagonist, in the doses of 3 to 30 mg/kg, intravenously, was found to have no significant effect on the acid response to baclofen. However, GABA-analogues (MOPS and ABA; 10-30 mg/kg, i.v.) and lipophilic GABA derivatives structurally related to beta-amino acids (APPA and APHA; 30 mg/kg, i.v.) significantly counteracted the secretagogue action of baclofen. Further experiments on APPA action showed that the antisecretory effect of APPA could be overcome by higher doses of baclofen. APPA did not affect bethanechol stimulated acid secretion. These results suggest that the secretagogue action of baclofen is independent to GABAA- and GABAB-receptors and that APPA may interact with baclofen in regulation mechanisms of acid secretion, although further investigations are necessary to define the mode of action of APPA on the GABA-ergic system.

Amino Acids↗
PubMed1991

Differences in the antisecretory actions of the proton pump inhibitor AG-1749 (lansoprazole) and the histamine H2-receptor antagonist famotidine in rats and dogs.

Antisecretory effects of a substituted benzimidazole, (+/-)-2-[[[3-methyl-4-(2,2,2-trifluoroethoxy)-2-pyridyl]methyl] sulfinyl]-1H-benzimidazole (AG-1749) were compared with those of a histamine H2-receptor antagonist, famotidine. AG-1749 inhibited acid formation regardless of the stimulant in isolated canine parietal cells, while famotidine inhibited the histamine-stimulated acid formation selectively. In pylorus-ligated rats, AG-1749 suppressed basal acid secretion, histamine-, bethanechol-, pentagastrin-, 2-deoxy-D-glucose- and stress (restraint and water-immersion)-induced acid secretion; ID50 values were 1.0-6.0 mg/kg. On the other hand, famotidine only partially inhibited the acid secretion induced by 2-deoxy-D-glucose or stress, although it suppressed the acid secretion stimulated by other secretagogues several times more potently than AG-1749. The antisecretory effect of AG-1749 lasted longer than that of famotidine, especially in the case of bethanechol-stimulated acid secretion. In Heidenhain pouch dogs, both AG-1749 and famotidine potently inhibited histamine-, bethanechol-, pentagastrin- and peptone meal-stimulated acid secretion, but the inhibitory effect of famotidine was short-lived in the case of bethanechol- and pentagastrin-stimulated acid secretion. These results suggest that AG-1749 persistently inhibits acid secretion induced by both peripheral and central stimuli and suggest that the antisecretory effect of famotidine depends on the nature of the stimuli.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1992

L-365,260, a potent CCK-B/gastrin receptor antagonist, suppresses gastric acid secretion induced by histamine and bethanechol as well as pentagastrin in rats.

We evaluated the effects of a potent cholecystokinin (CCK)-B/gastrin receptor antagonist, L-365,260 (3R(+)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepin - 3-yl)-N'-( 3-methylphenyl) urea); a selective CCK-A receptor antagonist, devazepide (L-364,718); and cimetidine on gastric acid secretion induced by pentagastrin, histamine and bethanechol in anesthetized rats. We also evaluated the effects of L-365,260 and cimetidine on acid secretion in pylorus-ligated rats. Intravenous administration of L-365,260, L-364,718 and cimetidine dose-dependently reduced acid secretion induced by pentagastrin (20 nmol/kg/hr), with ED50 values of 0.63, 19.1 and 2.5 mumol/kg, respectively. Of interest was the finding that L-365,260, like cimetidine, dose-dependently inhibited acid secretion induced by histamine (100 mumol/kg/hr) and bethanechol (5 mumol/kg/hr) with ED50 values of 5.9 and 4.3 mumol/kg, respectively. L-364,718, even at 30 mumol/kg, i.v., had only a slight effect on histamine- or bethanechol-induced acid secretion. Gastric acid secretion was suppressed by treatment with L-365,260 (3-100 mumol/kg, i.v.) and cimetidine (11.9-396.4 mumol/kg, i.v.) in pylorus-ligated rats, with ED50 values of 13.3 and 96.9 mumol/kg, respectively. These results indicate that L-365,260 suppresses acid secretion induced by histamine and bethanechol in rats and that the gastrin receptor plays an important role in acid secretion in pylorus-ligated rats.

Animals↗
PubMed1983

Gastroesophageal reflux causing stridor.

We describe an infant with stridor associated with gastroesophageal reflux (GER). This is the first report in which there is clear documentation by pH probe of a temporal association between individual episodes of GER and stridor. We review the literature and speculate on the relationship between these two phenomena. GER should be considered in patients with stridor.

Bethanechol Compounds↗
PubMed1982

Islet-activating protein (IAP) reduces bethanechol-stimulated release of pancreatic polypeptide in the dog.

The effect of islet-activating protein (IAP) purified from culture medium of Bordetella pertussis was examined in dogs. This was assessed by the levels of pancreatic polypeptide (PP) as well as the responses of plasma insulin and glucagon to a parasympathomimetic agent, bethanechol. Plasma responses of these pancreatic hormones were measured before and 5 days after IAP injection. Although IAP had no significant effect on the bethanechol-stimulated increase in plasma glucose, insulin and glucagon, the PP response to bethanechol was significantly reduced after IAP treatment compared with that before IAP (p less than 0.05). In conclusion, IAP significantly and selectively reduced bethanechol-stimulated PP release in the dog although the mechanism remained to be elucidated.

Animals↗
PubMed1985

Differences between negative chrono-, dromo- and inotropic actions of cholinomimetics in the dog isolated atrium.

Both bethanechol and physostigmine produced dose-dependent negative chrono-, dromo- and inotropic effects in the dog isolated atrial preparation. Within a relatively small dose of bethanechol and physostigmine, negative inotropic effect was clearly induced but no significant chrono- and dromotropic changes were observed. With a relatively large dose, the two cholinomimetics caused negative chrono-, dromo- and inotropic effects. The order of the negative actions of the drugs in % changes was inotropism greater than dromotropism greater than or equal to chronotropism. These results indicate that pacemaker activity, sinoatrial conductivity and atrial contractility may be differentially sensitive to actions of cholinomimetics.

Animals↗
PubMed1976

[Effect of selective proximal and truncal vagotomy on canine gastric electrical activity (author's transl)].

Alterations in the electrical activity of the stomach were studied in 40 unanesthetized dogs with intact vagal innervation, with selective proximal vagotomy (SPV) and with truncal vagotomy (TV) using a chronically implanted unipolar needle electrodes. The basic electrical rhythm (BER) of the normal canine stomach occurred regularly in the frequency of 4.5 to 5.5 cycles per minutes with a waxing and waning of initial and second potentials repeated in every 5 to 6 minutes. After SPV, irregular BER was observed occasionally within a few days postoperatively. After TV, irregularity of BER was more marked and frequent for the first 2 weeks. Subcutaneous administration of bethanechol chloride or histamine decreased the frequency of regular BER and increased the magnitude of second potentials equally in any dog of the control, SPV and TV groups. Similar changes were observed after feeding of the canned meat. Insulin-induced hypoglycemia increased the magnitude of antral second potentials in either control or SPV dogs. In contrast, TV dogs revealed repetition of initial potentials shortly after intravenous adminstration of insulin, but failed to show any changes relevant to hypoglycemia.

Animals↗
PubMed1982

Neuro-pharmacologic studies on neurogenic bladder after radical hysterectomy.

Miction function of patients who had had radical hysterectomy was investigated neuro-pharmacologically. The patients were divided into two groups according to the operation, with or without preservation of the plexus pelvicus, and bladder and urethral functions were compared by the bethanechol test and phentolamine test. The group with transected plexus pelvicus showed neurogenic bladder with impairment of functions of parasympathetic and sympathetic nerves and the preserved group showed much less impairment in functions of both nerves.

Adult↗
PubMedDate not supplied

The treatment of pheochromocytoma associated with pseudo-obstruction and perforation of the colon, hepatic failure, and DIC.

The case of a 59-year-old man with paralytic ileus (pseudo-obstruction) associated with pheochromocytoma is reviewed. Paralytic ileus is believed to have been the result of overstimulation of alpha and beta receptors on the intestine by catecholamines. Phentolamine, bunazocin, propranolol, bethanechol and midaglizole in single administrations or in combination were administered. Phentolamine infusion clearly relieved the symptom, but ileus recurred, and the patient died of respiratory failure, liver dysfunction and disseminated intravascular coagulation syndrome. The significant role of catecholamines in causing these symptoms is discussed, and the management of this relatively rare complication is reviewed.

Adrenal Gland Neoplasms↗
PubMed1982

Desensitization of the muscarinic receptor controlling action potential of bullfrog atrial muscles.

Action potentials of the bullfrog atrial muscle, being depressed by carbachol in concentrations of (1-5) X 10(-7) M, were found to show a slow recovery when application of the drug was sustained. The rate of onset of recovery largely varied depending on individual preparations. The recovery of action potentials was neither due to changes in the ionic distribution across the membrane nor to a secondary action of catecholamine which was released by the nicotinic action of carbachol on sympathetic nerve terminals. These results suggested that the muscarinic ACh receptor responsible for the depression of action potentials showed desensitization to the action of its agonist. The slow inward current recorded by the voltage-clamp experiment showed a decrease and subsequent slow recovery in the presence of carbachol. This suggested that the muscarinic ACh receptor associating with the ionic channel of the slow inward current showed desensitization. It may be suggested on the basis of these experimental results that 1) the muscarinic ACh receptor of bullfrog atrial muscle may compose a receptor-ionic channel complex (RICC) with voltage-dependent CA2+ channel and 2) the molecular reaction between this RICC and agonist may be comparable to that occurring in the nicotinic RICC of the frog end-plate.

Acetylcholine↗