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At least 145 records · Page 8Linked to original sources
PubMed1982

Effect of isoprenaline on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of isoprenaline on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility for both frequency and strength. Isoprenaline, a beta 1- and beta 2-agonist, was used alone and in conjunction with selective blockade of beta 1 and beta 2 receptors. The stimulated antral motility was dose-dependently inhibited by isoprenaline. The effect was significantly blocked by the beta 1 + beta 2-adrenoceptor blocker propranolol and by using in conjunction the beta 1-adrenoceptor blocker practolol and the beta 2-adrenoceptor blocker H 35/25. H 35/25 and particularly practolol reduced the effect of isoprenaline to some extent, but the reduction was not of statistical significance. This indicates that isoprenaline acts on antral motility through both beta 2 and beta 1 receptors. Dose-response experiments with five logarithmically increasing doses of bethanechol and one dose of isoprenaline showed inhibition of a non-competitive type.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of dopamine on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility with regard to both frequency and strength. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone. The alpha-adrenoceptor blocker phentolamine reduced the effect of dopamine to some extent, but the reduction was not of statistical significance. The dopamine-inhibited motility was not altered by the beta 1-adrenoceptor blocker practolol or the beta 1 + beta 2-adrenoceptor blocker propranolol. This indicates that dopamine acts on gastric antral motility predominantly through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, do not seem to be involved in the motility response. Dose-response investigations with five increasing doses of bethanechol and one dose of dopamine showed inhibition of a non-competitive type.

Adrenergic alpha-Antagonists↗
PubMed1985

Effect of somatostatin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of somatostatin on gastric acid secretion and gastric antral motility in conscious dogs with gastric fistula. Infusion of bethanechol stimulated dose-dependently acid secretion, whereas the frequency and strength of antral motility was maintained at a high level. Somatostatin inhibited dose-dependently the stimulated acid secretion, whereas the effect on antral motility was more complex, acting especially on the amplitude of the contractions. The effects of somatostatin were not altered by using alpha-adrenergic, beta-adrenergic, dopaminergic, and serotonergic blocking drugs. The dose-response kinetics with four doses of bethanechol with and without somatostatin showed inhibition of a non-competitive type for gastric acid secretion and of a competitive type for antral motility with regard to amplitude.

Adrenergic alpha-Antagonists↗
PubMed1975

Comparative effects of metoclopramide and bethanechol on lower esophageal sphincter pressure in reflux patients.

The effects of oral metoclopramide, 10 and 20 mg, bethanechol, 25 mg, and placebo on lower esophageal sphincter pressure (LESP) were studied in 15 men with symptoms of gastroesophageal reflux and basal LESP less than 11 mm Hg. Each drug produced a significant increase in LESP when compared to placebo. Metoclopramide, 20 mg, produced a greater increase than either metoclopramide, 10 mg, or bethanechol, 25 mg. Serum gastrin concentrations were not altered by any of the drugs. Side effects were unremarkable. The LESP increasing effect of metoclopramide might be useful in treatment of gastro-esophageal reflux.

Administration, Oral↗
PubMed1991

General pharmacology of the four gastrointestinal motility stimulants bethanechol, metoclopramide, trimebutine, and cisapride.

The pharmacological profile of bethanechol (CAS 674-38-4), metoclopramide (CAS 364-62-5), trimebutine (CAS 39133-31-8) and cisapride (CAS 81098-60-4) was studied in a series of simple pharmacological tests in rats and dogs. Bethanechol stimulated both gastric emptying and intestinal propulsion but displayed also the well-known behavioral effects of a direct muscarinic acetylcholine receptor agonist. Metoclopramide showed the profile of a centrally active dopamine D2 antagonist. In addition, metoclopramide displayed a stimulant effect on spontaneous gastric emptying in rats, an effect that could not be related to dopamine D2 antagonism. The only effect observed with trimebutine was protection from castor oil diarrhea, probably due to its reported interaction with peripheral opiate receptors. Cisapride was a potent stimulant of gastric emptying in rats, 7 times more potent than metoclopramide. Cisapride was also a very specific gastrokinetic, over a large dose range (specificity ratio: greater than or equal to 20) devoid of effects indicative for direct interaction with dopamine or acetylcholine receptors. The relationship between the differential activity profiles of the compounds in the present study and differences in their mechanism of action and side-effect liability is discussed.

Animals↗
PubMed1979

Acid secretion and mucosal cyclic nucleotide content of the guinea pig isolated stomach during bethanechol stimulation.

Acid secretion and mucosal cyclic AMP and cyclic GMP content of guinea pig isolated stomach preparations were measured at various times after stimulation with bethanechol (1.7 X 10(-5) M). Significant increases in acid secretion were observed without changes in cyclic nucleotides. Pre-incubation of the tissues with theophylline (10(-3) M) increased acid secretion and nucleotide content. An additional increase in acid secretion was then obtained with bethanechol in these tissues but without further change in nucleotides. Carbachol (30 micrograms/kg) administered by interperitoneal injection to conscious guinea pigs also failed to change gastric mucosal cyclic nucleotides when the animals were sacrificed 15 min later. These results are discussed in relation to the mechanisms of cholinergic stimulation of gastric acid secretion.

Animals↗
PubMed1986

Bethanechol chloride can reverse erectile and ejaculatory dysfunction induced by tricyclic antidepressants and mazindol: case report.

A 43-year-old man who experienced profound dose-related erectile and ejaculatory dysfunction without loss of libido on three separate antidepressants and on the anorectic agent mazindol is described. Bethanechol chloride 20 mg p.o., taken 1 to 2 hours prior to sexual activity, permitted satisfactory erection and ejaculation during sexual intercourse, while the patient continued to take protriptyline or mazindol. Bethanechol chloride may prove to be of use in treating sexual dysfunction associated with drugs or conditions which increase sympathetic tone.

Adult↗
PubMed1983

Effects of four H2 histamine antagonists on bethanechol-stimulated acid and pepsin secretion in the dog.

In five gastric fistula dogs, each of four H2-receptor antagonists was given (at doses roughly equal to the dose inhibiting histamine stimulation at 50%) as background infusion to graded doses of i.v. bethanechol. We measured acid and pepsin secretion and gastrin release. All four compounds noncompetitively inhibited acid secretion, reducing maximum acid outputs by 50 to 70%. Two compounds, tiotidine and cimetidine, shifted the bethanechol dose-response for pepsin secretion about 30% to the right at midpoint without reducing maximum output significantly, whereas the other two, ranitidine and metiamide, did not alter the dose-response. Dose-dependent gastrin release was unaffected by cimetidine, an imidazole compound, and augmented by tiotidine and ranitidine, the two nonimidazole compounds. Actions on pepsin and gastrin are thus not related to H2-receptor effects. The uniform effect of the four antagonists on acid secretion indicates an essential interaction between cholinergic and histamine effects on the parietal cell, although we could not distinguish between prereceptor, receptor and postreceptor sites for such interaction.

Animals↗
PubMed1981

Influence of papaverine on bethanechol or OP-CCK stimulation of feline colonic muscle.

Papaverine relaxes smooth muscle from various organ systems throughout the body. The purpose of this study was to determine the effects of papaverine on colonic smooth muscle from the transverse colon of the cat. Myoelectrical activity was recorded with monopolar glass pore electrodes. Papaverine was administered alone and simultaneously with bethanechol or the octapeptide of cholecystokinin. Higher concentrations of papaverine (10(-4) M, 10(-5) M) abolished both slow-wave activity and migrating spike bursts. Lower concentrations of papaverine (10(-6) M) had no effect on slow waves or the migrating spike burst. Bethanechol (10(-6) M) or OP-CCK (4 x 10(-9) M, 4 x 10(-10) M) stimulated spike activity (p < 0.001). Papaverine (10(-6) M had a minimal effect on the increase in spike activity that occurred after octapeptide of cholecystokinin in a concentration of 4 x 10(-10) M (p < 0.05). Papaverine had no effect on the stimulation of the colonic smooth muscle by 4 x 10(-10) M octapeptide of the colonic smooth muscle by 4 x 10(-9) M octapeptide of cholecystokinin. These studies show that (a) papaverine can inhibit smooth muscle myoelectrical activity, (b) papaverine is a potent inhibitor of cholinergic stimulation of colonic smooth muscle, but (c) papaverine has a minimal effect on octapeptide of cholecystokinin stimulation of the isolated colonic smooth muscle.

Animals↗
PubMed1984

Effect of met-enkephalin on acid secretion from gastric fistulas and Heidenhain pouches in dogs stimulated by pentagastrin, pentagastrin plus bethanechol, or a meal.

In dogs with denervated Heidenhain pouches and gastric cannulas the authors studied the action of met-enkephalin on acid secretion stimulated by a liquid meal, pentagastrin or pentagastrin + bethanechol. Serum gastrin levels were determined during the feeding experiments. Meal-stimulated and pentagastrin-stimulated acid secretion from the gastric fistula were inhibited by met-enkephalin. A rise in pentagastrin-induced acid secretion was observed in the denervated stomach. No significant changes were observed in the postprandial acid response from the pouch to the meal, nor from the main stomach or the pouch during stimulation with pentagastrin + bethanechol. Gastrin release was decreased by met-enkephalin during the first hour following feeding and increased during the second hour. Our data indicate that met-enkephalin can either inhibit or stimulate acid secretion in dogs. The inhibition occurs only in the innervated fundic mucosa, and might be explained by a decrease in gastrin release and by a decrease in vagal tone.

Animals↗
PubMed1981

Effect of bethanechol or vagal nerve stimulation on ileocecal sphincter pressure in the cat.

Ileocecal sphincter pressure was studied in the cat, using an open-tipped perfused catheter system. Ileocecal sphincter pressure was measured under basal conditions and in response to bethanechol or direct vagal nerve electrical stimulation. The pressure was 26.1 +/- 5.0 mmHg basally, and was unaltered by section of either or both cervical vagi (p less than 0.05). Peripheral cervical vagal stimulation gave a 9.1 +/- 1.1 mmHg increase in ileocecal sphincter pressure (p less than 0.05) but central stimulation had no effect on ileocecal sphincter pressure. The ileocecal sphincter response to peripheral vagal nerve stimulation was antagonized completely by propranolol or phentolamine. Bethanechol gave a dose-response increase in ileocecal sphincter pressure with a maximal response of 18.0 +/- 2.9 mmHg at 50.0 microgram/kg (p less than 0.01). The ileocecal sphincter relaxed with ileal distension and contracted with colonic distension. These studies indicate that (a) the ileocecal sphincter shows an excitatory response to vagal stimulation and cholinergic agonists; (b) basal ileocecal sphincter pressure is independent of the vagi; (c) ileocecal sphincter inhibition can be initiated by ileal distension but not by vagal stimulation.

Animals↗
PubMed1990

Intracerebroventricular bethanechol for Alzheimer's disease. Variable dose-related responses.

Five male patients participated in a pilot open-label study of dose-related aspects of response to intracerebroventricular bethanechol in Alzheimer's disease. No patient had remission of symptoms, but three patients improved symptomatically and on tests of memory. Improvement was evident over a restricted range of doses for each subject, and symptoms were worse at doses below and above the optimal range. There was little overlap in the range of doses producing improvement among these three. Two patients had no consistent improvement in memory, and agitation, depression, paranoia, and seizures developed during treatment. Qualitative differences and variability in dosages producing responses complicate the identification of true drug response in the treatment of Alzheimer's disease.

Alzheimer Disease↗
PubMed1994

Cholinergic dysfunction in Shy-Drager syndrome: effect of the parasympathomimetic agent, bethanechol.

To determine the frequency, severity and organ distribution of cholinergic dysfunction in the Shy-Drager syndrome, eleven patients were prospectively studied. In addition to documenting adrenergic insufficiency, a battery of twelve tests was employed to assess cholinergic function. Six tests demonstrated pupillary, lacrimal, salivary, urinary bladder, sexual and sudomotor dysfunction in the majority of patients. Cardiac vagal function as studied by the heart rate response to deep breathing, the Valsalva manoeuvre, cold face test, apnoeic facial immersion and atropine test was affected in all patients. Oesophageal motility was abnormal in six patients. Cholinergic dysfunction in patients with the Shy-Drager syndrome was widespread but of variable severity and distribution. Subcutaneous administration of the parasympathomimetic agent bethanechol demonstrated hyperresponsiveness of lacrimal, salivary, oesophageal, bowel, bladder and sudomotor functions. It is suggested that the Shy-Drager syndrome is primarily a preganglionic cholinergic disorder with transsynaptic degeneration accounting for the development of postganglionic cholinergic as well as adrenergic dysfunction.

Aged↗
PubMed1983

Enhancement of desynchronized sleep signs after pontine microinjection of the muscarinic agonist bethanechol.

The question of which brainstem neuronal receptors can mediate cholinergic REM sleep induction was investigated by injecting the pure muscarinic agonist bethanechol via glass micropipettes in the pontine tegmentum of cats. The REM sleep enhancement was observed to be equally potent, equally dose-dependent and its appearance equally site-dependent as that previously observed with carbachol, a mixed muscarinic/nicotinic agonist. The results suggest that the pharmacological activation of muscarinic receptors in pontine neurons is sufficient to trigger REM sleep.

Animals↗
PubMed1992

Mucin and protein release in the rabbit jejunum: effects of bethanechol and vagal nerve stimulation.

The role of the vagus nerve and cholinergic mechanisms in the control of rabbit jejunal mucin and protein release was investigated in vivo. In anesthetized animals, a 10-cm segment of the jejunum was cannulated and perfused with saline. Perfusate was collected and analyzed for mucin (by immunoassay) and protein. Bilateral cervical vagotomy had no effect on basal mucin or protein output, suggesting that the vagus nerve does not exert a tonic control on jejunal macromolecule secretion. Electrical stimulation of the vagi did not alter mucin release, even in the presence of muscarinic cholinergic (scopolamine) or adrenergic (propranolol and phentolamine) blockade. In contrast, protein output increased significantly after vagal stimulation, an effect inhibited by scopolamine. In both vagotomized and vagally intact rabbits, the cholinergic agonist bethanechol (200 micrograms/kg intraperitoneally) induced a scopolamine-sensitive increase in both mucin and protein output. Predominantly serum proteins were released into intestinal perfusates after vagal or cholinergic stimulation. It is concluded that the extrinsic vagus nerve does not regulate rabbit jejunal mucin secretion in vivo and that cholinergic control of intestinal goblet cells is implemented entirely by the intrinsic enteric nervous system. In addition, cholinergic or vagal stimulation increases intestinal vascular and epithelial permeability, resulting in the passage of serum proteins into the lumen, possibly by opening tight junctions and paracellular pathways.

Animals↗
PubMed1988

Bethanechol supersensitivity test, rhabdosphincter electromyography and bulbocavernosus reflex latency in the diagnosis of neuropathic detrusor areflexia.

A total of 57 patients with neuropathic or nonneuropathic detrusor areflexia was studied with the bethanechol supersensitivity test, electromyography of the urethral rhabdosphincter and bulbocavernosus reflex latency. The sensitivity of these tests in detecting neuropathic areflexia was 90, 87.5 and 78.1 per cent, respectively, and the specificity was 95.6, 76 and 80 per cent, respectively. When all 3 tests were performed together the combined accuracy approached 100 per cent. These combined tests are useful in the diagnosis of patients with equivocal bladder neuropathic conditions and in those with subtle neurological lesions.

Adolescent↗
PubMed1983

Malacoplakia of the bladder: a case report of resolution with bethanechol, trimethoprim-sulfamethoxazole and ascorbic acid.

Malacoplakia is a granulomatous disease that most frequently involves the urinary tract but also may involve the genital tract, gastrointestinal tract and retroperitoneum. It is believed to be infectious in origin, secondary to a deficiency of intracellular lysosomal digestion, and heretofore considered a chronic problem. We report a case of malacoplakia of the bladder, which was treated successfully with a combination of bethanechol, trimethoprim-sulfamethoxazole and ascorbic acid.

Anti-Infective Agents, Urinary↗