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At least 73 records · Page 4Linked to original sources
PubMed1985

Effects of sham feeding, bethanechol, and bombesin on somatostatin release in dogs.

In seven conscious dogs with esophagostomies and gastric cannulas, the acid, gastrin, and somatostatinlike immunoreactivity (SLI) responses to 5-min sham feeding with or without pretreatment with atropine sulfate (20 and 100 micrograms/kg) were measured. The responses to bethanechol (100 micrograms X kg-1 X h-1), to bombesin (0.5 micrograms X kg-1 X h-1) with or without pretreatment with atropine sulfate, and to a combined stimulation with bethanechol and bombesin were also measured. Sham feeding resulted in an increase in plasma SLI concentration (basal level, 20.4 +/- 4.2 pg/ml; maximally stimulated level, 46.8 +/- 5.6 pg/ml; P less than 0.01). After the injection of atropine the integrated SLI response to sham feeding was significantly decreased but not suppressed. Infusion of bethanechol did not alter SLI plasma levels. Bombesin infused alone increased the plasma SLI concentration (basal level, 15.6 +/- 2.3 pg/ml; maximally stimulated level, 55.6 +/- 10.3 pg/ml; P less than 0.01). The integrated SLI response to bombesin was significantly decreased by atropine but not significantly changed by bethanechol. These studies show that sham feeding and bombesin release somatostatin. They suggest that somatostatin release is largely under vagal-cholinergic control.

Animals↗
PubMed1988

Intraventricular bethanechol infusion for Alzheimer's disease: results of double-blind and escalating-dose trials.

Ten patients with biopsy-proven Alzheimer's disease (AD) received low-dose (0.35 mg/d) intraventricular bethanechol, a muscarinic agonist, and saline placebo in a 24-week double-blind crossover design. Eight of these ten patients later participated in an open escalating-dose (to 1.75 mg/d) trial of bethanechol. Patients' drug responses were assessed by neuropsychological examination and informant measures of activities of daily living, mood disturbance, and abnormal behavior. Bethanechol appears to have a narrow therapeutic window for positive effects; low doses did not reliably alter patient functioning, moderately increased doses appeared to have a palliative effect on patient mood and behavior, and the highest dose was detrimental to patient functioning. Bethanechol does not appear to ameliorate the dementia of AD, but may exert a mildly positive effect on patient behavior and mood.

Aged↗
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↗
PubMed1991

Bethanechol and phenylephrine responses in canine inferior vena cava and abdominal aorta.

Both canine inferior vena cava and abdominal aorta showed a concentration dependent increase of contraction in response to phenylephrine; however, inferior vena cava contracted in response to bethanechol but abdominal aorta did not respond to bethanechol. When the inferior vena cava was preconstricted with 1 x 10(-3)M bethanechol, low concentrations of phenylephrine (1 x 10(-7)M to 1 x 10(-6)M) induced relaxation, but relaxation by phenylephrine of abdominal aorta pretreated with 1 x 10(-3)M bethanechol did not occur.

Animals↗
PubMed1985

Bethanechol versus antiacids in the treatment of gastroesophageal reflux.

To compare the efficacy of bethanechol in the treatment of gastroesophageal reflux with that of antiacids, a prospective, cross-over study was undertaken, in which 20 affected infants and children were randomized into two groups on 6-week alternate bethanechol and antiacids oral medication. Patients were evaluated clinically and by esophageal pH-metry before and after each treatment. Clinical score amelioration was achieved earlier than reflux number reduction and with similar incidence in both groups of patients, irrespectively to the initial medication; moreover, the differences in the degree of improvement between the two groups after either treatment were not found to be significant. These results fail to show that bethanechol is more effective than antiacids in controlling gastroesophageal reflux; moreover, bethanechol is more difficult to administer and offers a higher rate of undesired side effects.

Aluminum Hydroxide↗
PubMed1982

Bethanechol or cimetidine in the treatment of symptomatic reflux esophagitis: a double-blind control study.

We conducted a double-blind study to compare the effectiveness of oral bethanechol chloride or cimetidine in treating reflux esophagitis to evaluate the drugs' effects on the symptoms of esophagitis and its verification by endoscopy. Forty-three patients were treated with either 300 mg of cimetidine or 25 mg of bethanechol chloride, each administered four times a day for six weeks. In addition to this drug treatment, the patients all received conventional medical therapy. Patients who were treated with either of the two drugs experienced a decrease in symptoms and less severe endoscopic lesions. While cimetidine treatment resulted in complete endoscopic healing in 15 of 22 patients, bethanechol treatment resulted in the same healing in 11 of 21 patients. During therapy, neither endoscopic lesions or symptoms worsened. Our study indicated that either cimetidine or bethanechol is an effective drug in treating reflux esophagitis. The effects of the two drugs can be favorably compared.

Administration, Oral↗
PubMedDate not supplied

Influence of bethanechol on retained particles deposited on the first bifurcation of rabbits.

Retention of 4 micron 51Cr labelled Teflon particles administered to nine male rabbits via trachea was measured externally. About 5 microliter of a suspension with a particle concentration of 40 mg X ml-1 was deposited on the first bifurcation through a fiberoptic bronchoscope under urethane anesthesia. Over a period of two weeks, the rabbits were exposed twice, under the influence of the cholinergic drug bethanechol chloride and in a control examination. The time period during which 90% of deposited particles had cleared was significantly shorter in the presence of bethanechol (16 h) than in the control experiment (70 h). The magnitude of the fraction which cleared within the first hour did not differ significantly for drug administration and control, being 39.0% and 36.8%, respectively. The fraction which did not clear within the first hour tended (p = 0.1) to clear faster, half-time 10.4 h, when bethanechol chloride was given than it did in the controls, half-time 31.3 h. A reasonable interpretation of the results is that the cholinergic compound, bethanechol, increases bronchial secretion, which results in a reversed movement of the particles that previously penetrated the mucous layer, back to the mucous layer.

Animals↗
PubMed1976

Bethanechol chloride in neurogenic bladder dysfunction.

Representative case summaries of patients with different types of neurogenic bladder diagnosed by combined cystometric-perineal electromyography and treated with bethanechol (Urecholine) are presented. Determination of the activity of the periurethral striated muscle in relation to bladder dysfunction is extremely important in the selection of patients for bethanechol therapy. In the absence of structural obstruction, bethanechol can be used in patients with (1) the early phase of coordinated reflex neurogenic bladder and sphincter when there is incomplete bladder emptying due to feeble or unsustained detrusor contractions, (2) recovery phase of spinal shock when the periurethral striated muscle has recovered and is under voluntary control, (3) incomplete motor paralytic bladder with coordinated sphincter, and (4) sensory paralytic bladder with decompensation. The bethanechol regimen will vary in accordance with the type of bladder being treated.

Achondroplasia↗
PubMed2006

A randomized phase III prospective trial of bethanechol to prevent radiotherapy-induced salivary gland damage in patients with head and neck cancer.

The aim of this study was to verify whether the use of bethanechol during radiotherapy (RT) for head and neck cancer (HNC) prevents radiation-induced xerostomia and salivary flow reduction. Patients that would begin RT were randomly allocated into bethanechol (group 1) or artificial saliva (group 2). Whole resting saliva (WRS) and whole stimulated saliva (WSS) were collected from all the patients at the following four stages: baseline, during, immediately after, and at least two months after the end of RT. Xerostomia was assessed by a subjective visual analogue scale (VAS), and by asking patients whether they felt dry mouth. Forty-three patients were randomized into this trial. The use of bethanechol during RT for HNC cancer was associated with significantly higher WRS immediately after RT (p=0.03) in comparison to a similar cohort of patients who had not received bethanechol.

Adult↗
PubMed1980

Coronary vasoconstriction by locally administered acetylcholine, carbachol and bethanechol in isolated, donor-perfused, rat hearts.

1 Experiments were carried out on rat isolated heart preparations in which the coronary vasculature was perfused through the aorta at a constant flow rate with arterial blood from donor animals. Single doses of drugs were injected into the aortic cannula. 2 Small doses of acetylcholine, carbachol or bethanechol decreased perfusion pressure (PP) without markedly affecting left ventricular pressure (LVP) and heart rate (HR); larger doses of these drugs increased PP (vasoconstriction), and decreased LVP and HR in a dose-dependent manner. 3 Acetylcholine, carbachol and bethanechol had almost no effects when perfused through the aorta in such a way as to exclude the coronary vessels. 4 Coronary vasoconstriction in response to acetylcholine, carbachol and bethanechol was not significantly affected by reserpine pretreatment, phentolamine or hexamethonium, but was antagonized by small doses of atropine. 5 From these results it is concluded that in the coronary vasculature of the rat, the receptors involved in the vasoconstrictor actions of acetylcholine carbachol and bethanechol are muscarinic.

Acetylcholine↗
PubMed1999

Topical diltiazem and bethanechol decrease anal sphincter pressure without side effects.

BACKGROUND: Topical nitrates lower anal sphincter pressure and heal anal fissures, but a majority of patients experience headache. The internal anal sphincter has a calcium dependent mechanism to maintain tone, and also receives an inhibitory extrinsic cholinergic innervation. It may therefore be possible to lower anal sphincter pressure using calcium channel blockers and cholinergic agonists without side effects. AIMS: To investigate the effect of oral and topical calcium channel blockade and a topical cholinomimetic on anal sphincter pressure. METHODS: Three studies were conducted, each involving 10 healthy volunteers. In the first study subjects were given oral 60 mg diltiazem or placebo on separate occasions. They were then given diltiazem once or twice daily for four days. In the second and third studies diltiazem and bethanechol gels of increasing concentration were applied topically to lower anal pressure. RESULTS: A single dose of 60 mg diltiazem lowered the maximum resting anal sphincter pressure (MRP) by a mean of 21%. Once daily diltiazem produced a clinically insignificant effect but a twice daily regimen reduced anal pressure by a mean of 17%. Diltiazem and bethanechol gel produced a dose dependent reduction of the anal pressure; 2% diltiazem produced a maximal 28% reduction, and 0.1% bethanechol a maximal 24% reduction, the effect lasting three to five hours. CONCLUSIONS: Topical diltiazem and bethanechol substantially reduce anal sphincter pressure for a prolonged period, and represent potential low side effect alternatives to topical nitrates for the treatment of anal fissures.

Administration, Oral↗
PubMed1982

Induction of wet dog shakes by intracerebroventricular bethanechol in rats. Antagonism by neurotransmitter receptor blockers.

Bethanechol chloride, administered intracerebroventricularly, induces a characteristic wet dog shake (WDS) response in rats in a dose-related manner. WDS induced by bethanechol at the dose of 100 micrograms was antagonized by atropine, scopolamine and spiperone (muscarinic cholinergic and dopaminergic antagonists, respectively), whilst metergoline, methysergide, phentolamine, propranolol and bicuculline (serotonergic, alpha-adrenergic, beta-adrenergic and GABA-ergic antagonists) fail to inhibit this effect. The present experiments show that the shaking response may be produced by bethanechol, a potent muscarinic agent administered by the intracerebral route, and suggest that bethanechol-induced shaking behavior in rats may be a useful animal model for delineating agents with antimuscarinic activity.

Animals↗
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↗
PubMedDate not supplied

Modulation of urethral alpha-sympathetic by parasympathetic before and following bethanechol chloride injection.

INTRODUCTION AND OBJECTIVES: Chagas' disease causes specific parasympathetic denervation and in its digestive clinic form promotes also functional alterations in bladder. Thus, the aim was to investigate the existence of balance between sympathetic and parasympathetic systems in lower urinary tract, as occurs in other organs. We verified the urethral closing pressure before and following parasympathetic stimulus. PATIENTS AND METHODS: For that, the urethral closure pressure was studied before and after the injection of 5 mg of bethanechol chloride subcutaneously in 28 voluntary female patients, divided into 4 groups. The constitution of theses groups was: A) normal control = 6 patients; B) Chagas' disease with positive serology only = 5 patients; C) Chagas' disease with cardiac disease = 6 patients, and D) Chagas' disease with digestive disease and vesical hyporeflexia = 11 patients. Urethral profilometry was performed through perfusion urethral catheter with a 6.5 ml/minute flow and a traction rate of 5 mm/minute. RESULTS: Means and standard deviations for urethral closure pressure before bethanechol chloride were respectively: group A = 67.3 +/- 7.1; group B = 69.2 +/- 7.4; group C = 95.8 +/- 5.1; group D = 82.1 +/- 8.4. After bethanechol chloride they were: group A = 66.0 +/- 6.6; group B = 77.0 +/- 7.6; group C = 98.3 +/- 8.8; group D = 45.9 +/- 6.2. The Kruskal Wallis statistical test did not show statistically significance difference between groups A, B, C. However, it was statistically significant between groups C and D with p = 0.003. Wilcoxon test showed p = 0.001, only for values in group D before and following bethanechol chloride. CONCLUSIONS: Chagas' disease in its intestinal form seems to alter urethral function as well. Parasympathetic stimulation decreased urethral pressure, indicating potential modulation by the parasympathetic system over the sympathetic system.

Journal Article↗
PubMed1994

The muscarinic agonist, bethanechol, enhances GABA-induced inhibition of Purkinje cells in the cerebellar cortex.

An important function of cholinergic projections to the cerebellar cortex may be to modulate the effects of classical afferent inputs to the cerebellar cortex. This hypothesis is supported by the recent observation that cholinergic agonists act at muscarinic receptors in the cerebellar cortex to facilitate Purkinje cell responses to glutamate, the excitatory neurotransmitter of parallel fibers [Brain Res., 617 (1993) 28-36]. Since Purkinje cell excitability is influenced by inhibitory input from basket and stellate cells as well as by excitatory input from granule cells and climbing fibers, the present study investigated whether muscarinic agonists could also modify the Purkinje cell responses to GABA, the putative inhibitory transmitter of basket and stellate neurons. In anesthetized rats, microiontophoretic application of bethanechol produced a long-lasting enhancement of GABA-evoked inhibition of firing of Purkinje cells in the cerebellar vermis (22/25 cells) regardless of whether bethanechol increased, decreased or failed to alter the basal firing rate of the cell. The muscarinic antagonist scopolamine prevented the bethanechol-induced increase in the GABA response. It appears, therefore, that cholinergic activation of muscarinic receptors enhances not only the excitatory but also the inhibitory component of cerebellar cortex circuitry. Further experiments are required to investigate whether this combination of effects may potentiate the signal processing capabilities of the cerebellar cortex.

Action Potentials↗
PubMed1983

Relaxant effects of vasoactive intestinal peptide and bethanechol in cat intrapulmonary artery.

The relaxant actions of vasoactive intestinal peptide (VIP) and bethanechol were examined on ring segments of intrapulmonary artery (IPA) isolated from cat lung. On a molar basis, VIP was 75 times more potent than bethanechol; however, VIP was less efficacious than bethanechol in reversing phenylephrine induced tone. Responses to VIP were unaffected by pretreatment of the tissues with atropine, indomethacin or avian pancreatic polypeptide. These results suggest that VIP may participate in the regulation of pulmonary vascular smooth muscle tone through a potent relaxant action that occurs independent of muscarinic cholinergic receptor activation or liberation of prostaglandins.

Animals↗
PubMed1983

Modulation of rat pancreatic amylase secretion and muscarinic receptor populations by chronic bethanechol treatment.

F8P6effect of a chronic bethanechol treatment (12 mg X kg-1 X day-1 i.p., for 14 days) was investigated on pancreatic amylase secretion and muscarinic cholinergic receptors in the rat. Dispersed pancreatic acini were used to evaluate enzyme secretion and binding of [3H]N-methylscopolamine, [( 3H]NMS). The bethanechol treatment caused a 4 fold decrease in sensitivity of the pancreas for amylase release in the presence of carbamylcholine, the EC50 being shifted from 0.69 microM to 2.9 microM. Receptor concentration was reduced by 42%, from 3360 to 1930 fmol/mg DNA. The equilibrium dissociation constant (KD) of the receptors for the ligand remained unchanged at 0.17 nM. Binding analysis of carbachol on the muscarinic receptors in terms of two classes of binding sites indicated that the shift in the dose-response curve of amylase secretion was accompanied by modifications to the high and low affinity forms. The maximal number of high affinity sites remained the same while their affinity was greatly decreased from 0.24 to 6.1 microM. The low affinity form showed a moderate decrease in affinity from 34 to 150 microM but a large drop in their numbers from 2620 to 890 fmol/mg DNA. These results suggest that the shift in the amylase dose-response curve to carbamylcholine, noted following bethanechol treatment in vivo, could be coupled with the observed change in affinity of the two agonist forms of muscarinic receptor in the pancreas. However, gradual occupancy or formation of the high affinity form of muscarinic receptors by cholinergic agonist corresponds well with the gradual stimulation of amylase release.

Amylases↗
PubMed1994

A clinical trial of bethanechol in patients with xerostomia after radiation therapy. A pilot study.

The effects of bethanechol in the treatment of dry mouth were assessed in patients with xerostomia after radiation therapy to the head and neck. Bethanechol possesses muscarinic and nicotinic-cholinergic activity that likely accounts for its mode of action. Bethanechol (25 mg, three times daily) was not associated with significant side effects. Statistically significant increases in whole resting saliva (p = 0.003) and whole stimulated saliva (p = 0.001) were seen. In patients with pretreatment stimulated saliva volumes greater than resting saliva volumes, a positive response to subsequent use of the sialagogue was seen.

Bethanechol↗