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PubMed1986

Effect of serotonin on bethanechol-stimulated gastric acid secretion and gastric antral motility in dogs.

The purpose of the present study was to evaluate the effect of serotonin on bethanechol-stimulated gastric acid secretion and antral motility in conscious dogs with gastric fistula. Bethanechol stimulated the acid secretion dose-dependently and maintained the frequency and strength of the antral contractions at a high level. Serotonin inhibited the acid secretion dose-dependently, whereas the antral motility was stimulated. The acid inhibition was blocked by propranolol, and dose-response analysis showed inhibition of a non-competitive type. This study thereby shows that serotonin inhibits bethanechol-stimulated gastric acid secretion similarly to salmefamol (beta 2-adrenergic agonist)--that is, dose-dependently and non-competitively. Serotonin has been proposed to be a mediator of the beta-adrenergic influence on gastric function in vivo, but the counteracting effect of propranolol and the stimulatory effect of serotonin on motility contradict this hypothesis.

Animals↗
PubMed1978

The effects of norephedrine and bethanechol on the human urethral closure pressure profile.

In twelve women with urinary stress incontinence simultaneous measurements were made of the intravesical and intra-urethral pressures, including the urethral closure pressure profile (UCPP), before and after oral administration of norephedrine or subcutaneous injection of bethanechol. The investigations were carried out at various bladder volumes in the supine position and at bladder volume 300 ml in erect position. Irrespective of bladder volume or body position, norephedrine caused a statistically significant rise in maximum urethral pressure (MUP) and in maximum urethral closure pressure (MUCP). The intravesical pressure was not affected. After intravenous injection of phentolamine, MUP and MUCP fell to levels below the original readings, but here too the intravesical pressure was unaffected. Injection of bethanechol was followed by significant increase in the intravesical pressure, irrespective of bladder volume or body position. There were no consistent changes in the intra-urethral pressure. As a consequence of the rise in intravesical pressure, however, the MUCP fell slightly. The results of the study suggest that orally administered norephedrine causes an increase in the MUCP in women with stress incontinence of urine, an increase that may prove therapeutically useful. Bethanechol, in doses that significantly increased intravesical pressure, did not alter the intra-urethral pressure.

Administration, Oral↗
PubMed1982

In vitro effect of acetylcholine and bethanechol on the contractions of the human detrusor muscle. Influence of prostaglandins.

The effects of acetylcholine and bethanechol on the basal resting tone of the isolated detrusor muscle were explored. It was observed that the tone was augmented by both agents. On the other hand, in the presence of prostaglandin (PG)-inhibitors the dose-response curve of acetylcholine shifts to the right. PGF 2 alpha (10(-10)M) but not PGE2 (10(-10)M) completely blocked the inhibitory effect of PG-inhibitors upon the inotropic effect of acetylcholine, without modifying the influence of bethanechol. After inhibitors of PG-synthesis, eserine abolished the inhibitory action of acetylcholine but did not change the influence of bethanechol. Our results suggest that endogenous PGs facilitate the action of acetylcholine through an increase in the concentration of the cholinergic neurotransmitter probably via an inhibition of the acetylcholinesterase activity.

Acetylcholine↗
PubMed1983

Effects of the sympathetic nervous system on bethanechol-induced elevation of gastric acid secretion and mucosal blood flow in rats.

Effects of stimulation of the sympathetic nervous system on the bethanechol-induced increase in gastric acid secretion and mucosal blood flow (MBF) were studied in anesthetized, gastric fistula rats. The gastric acid secretion and MBF were increased by i.v. infusion of a supramaximal dose of bethanechol (10.0 micrograms/kg/min). The bethanechol-induced gastric acid secretion was abolished by administration of atropine (0.1 mg/kg i.v.), but was not influenced by hexamethonium (2.0 mg/kg i.v.) in the dose which abolished the gastric acid secretion induced by vagus nerve stimulation. Stimulation of the splanchnic postganglionic (SP) nerve or infusion of norepinephrine was carried out under the steady, increased state of acid secretion and MBF. Stimulation of the SP nerve significantly reduced the gastric acid secretion but the MBF was little affected. Thus, the delta MBF/delta H+ ratio was significantly increased during this stimulation. Intravenous infusion of norepinephrine also reduced the acid secretion without affecting the MBF. The delta MBF/delta H+ ratio was also significantly increased during infusion of norepinephrine. Phentolamine, but not propranolol, abolished the inhibitory effects of SP nerve stimulation and infusion of norepinephrine on the gastric acid secretion. These results suggest that the SP nerve acts on the structures peripheral to the postganglionic parasympathetic nerve terminals and directly inhibits the parasympathetically stimulated gastric acid secretion through alpha adrenoceptors, independently of changes in the gastric MBF in rats.

Animals↗
PubMed1984

Facilitation of ganglionic response to bethanechol by repetitive stimulation of the preganglionic nerve.

Repetitive stimulation of the preganglionic nerve of the rat superior cervical sympathetic ganglion potentiates the amplitude of asynchronous firing elicited by the muscarinic agonist, bethanechol. The amplitude of stimulus-induced facilitation is not related to frequency of stimulation and occurs with a stimulation frequency of 10 Hz or greater. Facilitation, but not the asynchronous firing is reduced by lowering the temperature of the bathing solution. Dibutryl cyclic adenosine monophosphate and theophylline had no effect on asynchronous firing but reduced stimulus-induced facilitation. Neither dibutryl cyclic guanosine monophosphate up to 1 mM nor nitroprusside had any significant effect on bethanechol-induced asynchronous firing or stimulus-induced facilitation. Tetraethylammonium caused a 200% increase in stimulus-induced facilitation. Acetylcholine, in a concentration that elicited maximum nicotinic firing, had no effect on the magnitude of bethanechol-induced asynchronous firing. Increased Ca++, Mg++ or Mn++ reduced both asynchronous firing and stimulus-induced facilitation. It is concluded that facilitation is a result of transmitter release, possibly not acetylcholine.

Acetylcholine↗
PubMed1995

Ischemic preconditioning, adenosine and bethanechol protect spontaneously hypertensive isolated rat hearts.

The frequency of chronic hypertension among cardiac surgery patients implies that experimental therapies that protect normotensive myocardium will be more clinically relevant if they also protect chronically hypertensive myocardium. We tested the effectiveness of three experimental therapies that protect normotensive myocardium from ischemic injury in both normotensive (NTR) and spontaneously hypertensive (SHR) isolated Sprague-Dawley rat hearts. Post-ischemic recovery of ATP, left ventricular end diastolic pressure, developed pressure, negative and positive left ventricular dP/dt (-dP/dt and +dP/dt) and coronary flow (CF) were compared in ischemically preconditioned, adenosine-pretreated, bethanechol-pretreated and untreated NTR and SHR isolated rat hearts. The effect of time on our preparation was evaluated by comparison to NTR and SHR hearts maintained in vitro for equal duration but not subjected to an ischemic insult (N = 7, all groups). Preconditioning, adenosine and bethanechol significantly improved recovery of ATP, left ventricular end diastolic pressure, developed pressure, -dP/dt, +dP/dt and coronary flow in both NTR and SHR hearts (P < 0.001 vs. untreated, all comparisons). Although recovery was not so pronounced in SHR hearts, these results suggest that experimental therapies that protect normotensive myocardium also protect chronically hypertensive myocardium. The effect of adenosine and that of ischemic preconditioning were nearly identical, and both treatments were significantly more cardioprotective than bethanechol in both NTR and SHR hearts (P < .05 and P < .001, respectively). This result suggests that adenosine buildup is more important than muscarinic receptor stimulation as a mechanism of the protection afforded by ischemic preconditioning.

Adenosine↗
PubMed1996

Vascular responses to norepinephrine and bethanechol in isolated aortae from 2-month diabetic rabbits induced by alloxan.

The present study examined responses to norepinephrine and bethanechol in isolated aortae from 2-month diabetic rabbits induced by alloxan. Alloxan (100 mg/kg) was administered intravenously into the ear vein, and the blood glucose levels were estimated weekly for a duration of 2 months. The aortae from 2-month diabetic rabbits were removed and the aortic responses to norepinephrine and bethanechol were tested in vitro. The data showed that the aortic response to norepinephrine was increased but the aortic response to bethanechol was decreased in diabetic aortae; however, changes of responses were insignificant in comparing with those of the age-matched control aortae. It was speculated that a longer duration of diabetic development should be helpful to ensure a significant change of aortic response to vasoactive agents.

Alloxan↗
PubMed1993

Effects of atropine, glucagon, and bethanechol on urodynamics of continent cecal urinary reservoir before and after complete, partial, and sham detubularizations in dog.

Effects of muscarinic receptor blockade (atropine), stimulation (bethanechol), and bowel smooth muscle relaxant (glucagon) on the urodynamics of the continent cecal urinary reservoir in a tube form and after complete, partial, and sham detubularizations were studied using dogs. Complete detubularization significantly increased capacity and decreased spontaneous motor activity, whereas the other types of detubularization had no significant effects on them. Neither atropine nor glucagon had influence on the basal pressure, but they increased the capacity and the volume at which the first pressure wave appeared and decreased the wave amplitude. After detubularization glucagon further decreased uninhibited contractions while atropine totally abolished them. The highest capacity and lowest motor activity was gained when atropine or glucagon was given in cases with detubularized pouch demonstrating an additive effect of the detubularization and drug. Also, bethanechol increased the motor activity and decreased the volume in detubularized problem in a patient with a detubularized cecal pouch, orally administered anticholinergic or bowel smooth muscle relaxing drugs may be useful in management.

Animals↗
PubMed1990

Effects of two new pirenzepine analogs on the contractile response of the guinea-pig oesophageal muscularis mucosae to acetylcholine, bethanechol, histamine and high potassium.

The guinea-pig oesophageal muscularis mucosae was used to determine the affinity for muscarinic receptors of two new tricyclic compounds, DF 545 and DF 594, which are structurally related to pirenzepine. Both acetylcholine and bethanechol induced a concentration-dependent contraction of the muscularis mucosae. This contraction was competitively antagonized by DF 545 and DF 594 over the dose range 10(-7)-10(-5) M, while at higher concentrations both antagonists caused a depression of the maximal response to the cholinomimetics. The potency of DF 545 and DF 594 appeared to be comparable to that of pirenzepine and approximately 50 times lower than that of atropine. By comparing the affinities of DF 545 and DF 594 with those of selective antagonists (methoctramine and 4-DAMP) which discriminate between M2/M3 muscarinic receptor subtypes, it emerged that pirenzepine as well as DF 545 and DF 594 might act on M3 receptors, which seem to be predominant in the guinea-pig oesophageal muscularis mucosae. McN-A-343 exhibited no agonist activity while it acted as a competitive antagonist against acetylcholine and bethanechol. None of the compounds exhibited calcium antagonist properties. DF 545 inhibited the contractile responses to histamine, but DF 594 and pirenzepine did not.

Acetylcholine↗
PubMed1987

Divergent effects of bombesin and bethanechol on stimulated gastric secretion in duodenal ulcer and in normal men.

To further investigate differences in the responses of normals and patients with duodenal ulcer with respect to gastrin release and acid and pepsin secretion, we infused bombesin (1 microgram/kg X h) or bethanechol (40 micrograms/kg X h) during the middle hour of a 3-h infusion of pentagastrin and compared the results with a pentagastrin infusion without added drug. Pentagastrin dosage (0.1 microgram/kg X h) was set to give about half-maximal response, to detect either inhibition or further stimulation of gastric secretion, whereas the dose of bombesin was chosen to give maximal gastrin but less than maximal acid secretion. Serum gastrin and somatostatin were also measured. In all subjects tested, bethanechol produced no effects on acid, gastrin, or somatostatin release but increased pepsin output. By contrast, bombesin inhibited pentagastrin-stimulated acid output in all 6 normal men by an average of 55%, whereas it inhibited acid output in only 2 of the 9 men with duodenal ulcer. Serum gastrin increases after bombesin in duodenal ulcer were three to four times greater than in normals. Although bombesin stimulates acid only by releasing gastrin, we postulate that bombesin may also simultaneously limit acid and pepsin secretion and speculate that this effect could be mediated by bombesin-induced somatostatin release. The cause for differences between duodenal ulcer and normal remain speculative.

Adult↗
PubMed1988

Effect of bethanechol on glycolysis and high energy phosphate metabolism of the rabbit urinary bladder.

The urinary bladder, similar to other smooth muscles, utilizes glucose as one of its primary sources of metabolic energy. We have studied the effect of bethanechol on both glycolysis and high energy phosphate metabolism. The results can be summarized as follows: bethanechol administration in vitro stimulates a 30% decrease in intracellular glycogen, a 100% increase in lactic acid production, and an 80% increase in CO2 generation. Although there was a rapid and sustained decrease in the intracellular concentration of creatine phosphate, there was only a minor decrease in the intracellular concentration of ATP. There were no changes in adenine uptake or de novo ATP synthesis.

Adenine↗
PubMed1981

The effect of oral bethanechol chloride on voiding in female patients with excessive residual urine: a randomized double-blind study.

The usefulness of bethanechol chloride as a therapeutic adjunct in the treatment of patients with residual urine but no obstruction has been questioned. This study, in which oral bethanechol chloride was compared to a placebo in a randomized, double-blind fashion, does not show a significant short-term effect in female patients with persistent elevation in residual urine. No differences were seen in voided volume, residual volume, percentage residual volume, mean flow rate and intravesical pressure at 100 ml. volume and at maximal capacity when the treatment groups were compared to the group receiving the placebo.

Administration, Oral↗
PubMed1989

Effects of bethanechol and adreno-blockers on thermoregulation in spinal cord injury.

The authors report two cases of hypothermia due to a treatment associating Bethanechol and Adreno-Blockers. They emphasize the mechanisms of thermoregulation and discuss the pathophysiology of such hypothermia incidents. The most evident explanation is heat loss, principally mediated through Bethanechol, whereas mechanisms of heat preservation are prevented by Adreno-Blockers. Patients susceptible to this risk must be carefully monitored.

Adult↗
PubMed1986

Effect of bethanechol and metoclopramide on upper gastrointestinal motility in the kitten.

Gastroesophageal reflux (GER) during infancy is a disorder of unknown etiology which may be associated with abnormalities of upper gastrointestinal motor function. Bethanechol, a muscarinic agonist, and metoclopramide, a dopamine antagonist, have been utilized as pharmacologic agents in an attempt to improve upper gastrointestinal motility in this disorder. We have studied the effect of these agents on upper gastrointestinal motility in an infant model, the kitten. Bethanechol is found to greatly increase lower esophageal sphincter (LES) pressure and have no effect on esophageal peristaltic amplitude or gastric emptying of a liquid meal. Metoclopramide causes a small and nonsignificant increase in LES pressure, has no effect on esophageal peristalsis, and increases the rate of gastric emptying of a liquid meal. These results suggest that these two agents may have specific actions on the infant's upper gastrointestinal tract.

Animals↗
PubMed1986

Acute dystonic reaction to bethanechol--a direct acetylcholine receptor agonist.

Bethanechol is a direct agonist of the acetylcholine receptor that was recently introduced in the therapy of gastro-oesophageal reflux. Acute dystonic reactions to bethanechol were observed in a 10-month-old infant who also demonstrated similar dystonic reactions to dopamine receptor blocking agents of two different classes. This first report of acute dystonic reaction to cholinergic agonists in human is in accord with the current theories of the rôle of acetylcholine and dopamine in the pathogenesis of acute dystonic reactions.

Acute Disease↗
PubMed1984

Bethanechol prevents inhibition of gastric acid secretion by gastric inhibitory polypeptide.

Earlier studies of gastric inhibitory polypeptide (GIP) have shown that it is a powerful inhibitor of acid secretion in denervated gastric pouches. Other studies, however, have shown that it is a weak inhibitor in innervated stomach preparations. In this study we evaluated the inhibitory action of GIP in four dogs, each provided with both a vagally denervated (Heidenhain) pouch and a gastric fistula of the innervated stomach. The effect of intravenous infusion of pure porcine GIP (1 microgram X kg-1 X h-1) on pentagastrin dose response was studied with and without background infusion of bethanechol (25 micrograms X kg-1 X h-1). GIP powerfully inhibited pentagastrin-stimulated acid secretion from the Heidenhain pouch but not from the gastric fistula. The maximal inhibition was 76% for the Heidenhain pouch and 29% for the gastric fistula. Despite the attainment of high levels of circulating immunoreactive GIP (greater than 3,000 pg/ml) early after the onset of infusion of the peptide, inhibition occurred relatively late, suggesting that this action of GIP might be mediated by the release of some other substance(s). Background infusion of bethanechol totally abolished the inhibitory action of GIP in both the Heidenhain pouch and gastric fistula.

Animals↗
PubMed1989

Comparison of telenzepine, pirenzepine and atropine on gastric acid and pepsin secretion in response to histamine, pentagastrin, bethanechol, sham-feeding and feeding.

This study was designed to compare gastric antisecretory effects of telenzepine, a new antimuscarinic agent, with those of pirenzepine and atropine in dogs. None of these antimuscarinics affected gastric acid secretion induced by histamine but all of them caused a dose-dependent inhibition of acid secretion from the gastric fistula (GF) and Heidenhain pouches (HP) stimulated by pentagastrin and bethanechol, telenzepine being 5-9 times more potent than pirenzepine and equipotent with atropine. All antimuscarinics were also effective inhibitors of acid responses to sham feeding and ordinary feeding. The inhibitory effect of telenzepine and pirenzepine were not accompanied by any major alterations in plasma gastrin or somatostatin but those of atropine were related to significant increase in plasma gastrin and to significant decrease in plasma somatostatin levels, suggesting the involvement of M2 receptors in the cholinergic control of these hormones. All three antimuscarinics were effective inhibitors of pepsin secretion induced both from the GF and HP by all secretagogues used. Neither telenzepine nor pirenzepine administered in various doses affected the heart rate while atropine caused a significant increase in heart rate confirming that the former agents are selective M1 receptor antagonists. This study provides evidence that telenzepine is more potent than pirenzepine in the inhibition of gastric secretion induced by pentagastrin, bethanechol, sham-feeding and ordinary feeding and that, unlike atropine, it does not increase plasma gastrin responses to meat feeding. In fact, telenzepine and pirenzepine alike reduced plasma gastrin concentrations under these conditions. No influence of these antimuscarinics on plasma somatostatin levels was observed.

Animals↗
PubMed1989

Intracerebroventricular bethanechol chloride infusion in Alzheimer's disease. Results of a collaborative double-blind study.

The use of intracerebroventricular bethanechol chloride infusion in patients with Alzheimer's disease was first reported in 1984. An initial trial in four patients demonstrated the feasibility of this approach for cholinergic drug delivery to the brain, but objective improvement in cognitive function was not documented. A collaborative placebo-controlled double-blind crossover study has now been carried out in 49 patients with biopsy-documented Alzheimer's disease. The results demonstrate a statistical improvement in Mini-Mental State scores and significantly slower performance on Trails A testing during drug infusion. Other neuropsychological test scores were not similarly affected. The degree of improvement was not sufficient to justify further treatment of Alzheimer's disease patients by intracerebroventricular infusion of bethanechol chloride. The drug delivery system used in the study was well tolerated, with two irreversible complications in more than 50,000 patient days.

Alzheimer Disease↗