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PubMed2003

Pharmacological discrimination between muscarinic receptor signal transduction cascades with bethanechol chloride.

1. Muscarinic agonist specificity is limited, making it difficult to match receptor subtypes with signal transduction cascades that mediate ion channel modulation. We have characterized the inhibitory effects of two muscarinic agonists, oxotremorine-M (Oxo-M) and bethanechol chloride (BeCh), on Ca(2+) currents in neonatal rat superior cervical ganglion neurons. 2. Oxo-M-mediated (10 micro M) inhibition occurred via two signaling pathways. The first pathway inhibited whole cell peak currents, consisting primarily of N-type current, but not FPL 64176-induced, long-lasting tail currents, comprised entirely of L-type current. Inhibited currents displayed slowed activation kinetics and voltage dependence, characteristics of membrane-delimited inhibition. Current inhibition was blocked by the selective M(2) receptor antagonist, methoctramine (METH; 100 nM), or following pertussis toxin (PTX) pretreatment. 3. Activation of the second pathway inhibited both peak and long-lasting tail currents. This pathway was voltage-independent, PTX-insensitive, but sensitive to internal Ca(2+) chelator concentration. Muscarinic toxin 7 (MT-7, 100 nM), an irreversible M(1) receptor antagonist, eliminated this inhibition. Oxo-M (100 micro M) decreased L- and N-type channel activities in cell-attached patches, indicating that a diffusible second messenger is involved. 4. BeCh (100 micro M) also inhibited whole cell currents via the membrane-delimited pathway. Blocking M(4) receptors with 100 nM pirenzepine (in the presence of MT-7) had no effect, while antagonizing M(2) receptors with METH abolished inhibition. Concentrations of BeCh as high as 3 mM failed to inhibit either peak or long-lasting tail currents following PTX pretreatment. 5. These results indicate that BeCh may be an effective tool for selectively activating M(2) receptor stimulation of the membrane-delimited pathway.

Animals↗
PubMed2003

In vitro effects of cisapride, metoclopramide and bethanechol on smooth muscle preparations from abomasal antrum and duodenum of dairy cows.

The objective of this study was to investigate the effects of cisapride (CIS), metoclopramide (MET) and bethanechol (BET) on contractility parameters from smooth muscle preparations of the abomasal antrum and proximal duodenum of cows. Smooth muscle preparations were harvested shortly post-mortem from 42 healthy dairy cows, and concentration-response curves were performed by cumulative application of the drugs. Cisapride and MET did not have any significant effect on the contractility parameters studied, while BET induced a significant, concentration-dependent increase in basal tone (BT), mean amplitude (Amean), and area under the curve (AUC) in smooth muscle preparations from the abomasal antrum, but not from the duodenum. The effect of BET on BT was more pronounced in specimens with longitudinal orientation while the maximal obtainable effect (Vm) in Amean was more pronounced in circular-oriented preparations. Atropine (1 x 10-5 m) significantly inhibited the effect of BET, whereas pre-incubation with hexamethonium or tetrodotoxin (TTX) had no effect, suggesting that the effect was mediated by cholinergic receptors on the smooth muscle. The results may be relevant to diseases or disorders associated with gastric emptying and gastric hypomotility. Further investigations are warranted to investigate the potential ability of BET to enhance abomasal emptying of adult dairy cows.

Abomasum↗
PubMed2005

In vitro effects of bethanechol on equine gastrointestinal contractility and functional characterization of involved muscarinic receptor subtypes.

The goal of this study was to investigate the effect of bethanechol (BeCh) on contractility patterns of smooth muscle preparations of equine duodenum descendens, jejunum, caecum and pelvic flexure in vitro. Concentration-response relationships were developed for BeCh using in vitro assays with and without preincubation of muscarinic (M) receptor antagonists for M2 and M3 receptors. BeCh induced a significant, concentration-dependent increase in contractile response in equine intestine in specimens with circular orientation. The maximal effect was largest for jejunal specimens with no difference in EC50 within the different locations investigated. The M2 antagonist, AF-DX 116, caused a rightward shift of the concentration-response curve and the M3 antagonist, 4-DAMP (1,1-dimethyl-4-diphenylacetoxypiperidinium iodide), almost completely inhibited the effect of BeCh over the entire concentration-response curve. These data provide evidence that, although the effect of BeCh is predominantly mediated by M3 receptors, M2 muscarinic receptors also play a role in BeCh-induced contraction in specimens of equine intestine. The involvement of other muscarinic receptor subtypes cannot be excluded. Further studies are necessary to understand the effect of BeCh in vivo including diseased animals.

Animals↗
PubMed2004

Prostaglandin E2 and bethanechol in combination for treating detrusor underactivity.

OBJECTIVE: To test the hypothesis, in a prospective randomized double-blind study, that the combination of intravesical prostaglandin E2 (PGE2) and oral bethanechol chloride (BC) are additive or synergistic in improving bladder emptying, as they have been used alone for treating impaired detrusor contractility with little clinical benefit. PATIENTS AND METHODS: Nineteen patients with detrusor underactivity (17 men and two women) were eligible and randomized to one of two treatments. All had postvoid residual urine volumes (PVR) consistently of > 300 mL, most being reliant on clean intermittent self-catheterization (CISC). The experimental treatment group (nine patients) received once-weekly intravesical PGE2 (1.5 mg in 20 mL 0.9% saline) plus BC 50 mg four times daily, for a total of 6 weeks. The second group of 10 patients received a once-weekly instillation of saline together with placebo tablets, again for 6 weeks. RESULTS: Before treatment the median (interquartile range) PVR was 426 (405-480) mL for those receiving both drugs; this decreased to 325 (290-352) mL after completing the treatment (P < 0.015). In the placebo group the respective values were 576 (539-777) and 538 (350-775) mL (P = 0.09). Four of the patients receiving the active combination reported symptomatic improvement and were able to reduce the frequency of CISC. CONCLUSION: Although there was evidence of a pharmacological effect, BC and PGE2 had a limited therapeutic effect compared with placebo. Whilst we would not recommend this treatment as routine, it may be considered for the occasional treatment of a patient with detrusor underactivity.

Adult↗
PubMed1982

Effects of H2-receptor antagonists and anticholinoceptor drugs on gastric and salivary secretion induced by bethanechol in the anaesthetized dog.

1 The H2-receptor antagonists, ranitidine and cimetidine, have been compared with atropine and pirenzepine for their effects on gastric acid output, and on salivary secretion from the left parotid gland in the anaesthetized dog. Gastric and salivary secretions were elicited by intravenous infusion of bethanechol. 2 Atropine (0.3-1 microgram/kg) or pirenzepine (3-10 micrograms/kg) reduced both gastric and salivary secretions, pirenzepine showing little evidence of any selectivity for gastric secretion. 3 The H2-receptor antagonists, ranitidine (30-1000 micrograms/kg) and cimetidine (100-3000 micrograms/kg), selectively inhibited gastric secretion and even at relatively high dose levels did not alter salivary volume.

Anesthesia↗
PubMed1994

Differential effects of Na+, K(+)-ATPase inhibition by ouabain on acid secretory responses to histamine and bethanechol in the mouse isolated stomach.

1. The effect of Na+,K(+)-ATPase inhibition by ouabain on gastric acid secretion was studied in the mouse isolated whole stomach preparation. 2. Ouabain caused a transient enhancement of histamine-induced gastric acid secretion followed by an inhibitory phase. On the other hand, ouabain caused a rapid reduction of bethanechol-stimulated acid secretion without an enhancement phase. 3. In dibutyryl cyclic AMP-induced acid secretion, ouabain led to a transient increase in acid secretion followed by a fall, as was seen with the histamine stimulation. Ouabain caused a rapid reduction of A23187-induced acid secretion. 4. Ouabain by itself increased basal acid secretion, and thereafter slowly suppressed the acid secretion. 5. Atropine inhibited both the ouabain-induced enhancement of the stimulated gastric acid secretion and the ouabain-induced stimulation of basal acid secretion. 6. The present study showed that Na+,K(+)-ATPase inhibition by ouabain caused a phasic enhancement of the stimulated gastric acid secretion through release of endogenous acetylcholine when the secretagogues act via an intracellular cyclic AMP pathway. It also inhibited the stimulated acid secretion irrespective of secretagogues, probably through its inhibitory effect on Na+,K(+)-ATPase in the gastric parietal cell.

Animals↗
PubMed1985

Bethanechol decreases reaction time in senile dementia of the Alzheimer type.

Bethanechol, a muscarinic cholinergic agonist, was injected subcutaneously in eight cases of senile dementia of the Alzheimer type. Simple reaction time was measured before, 15 min and 30 min following the injection. Before injection, the patients had significantly longer reaction time than non-demented controls. A significant shortening of the reaction time was observed 15 min but not 30 min after injection. A second group of eight patients with senile dementia of the Alzheimer type, matched for age and mental impairment were injected with saline. No significant shortening of the reaction time was observed. These results suggest that the reaction time can be shortened by a muscarinic agonist in dementia of the Alzheimer type.

Adult↗
PubMed1975

The use of bethanechol chloride with tricyclic antidepressants.

The author describes the use of bethanechol chloride to relieve side effects, including salivary inactivation, constipation, and bladder inhibition, which result from the anticholinergic action of tricyclic antidepressants. He suggests that the use of cholinergic medication during antidepressant therapy may extend the use of the tricyclics to patients who find anticholinergic side effects especially troublesome.

Adult↗
PubMed1985

Effect of metoclopramide and bethanechol on gastric emptying in infants.

In a double-blind, placebo controlled study of 10 infants with upper gastrointestinal motor disorders, metoclopramide (1 mg/kg, intravenous) but not bethanechol (0.075 mg/kg, subcutaneous), significantly increased the fractional rate of gastric emptying following a 5% glucose meal. Infants were tested on 3 consecutive days with a phenol red dye-dilution technique which, if combined with acid titration of gastric samples, permits simultaneous measurements of gastric volume, fractional emptying rate, fluid output, and acid output. Metoclopramide increased the fractional emptying rate in eight of 10 infants (mean +/- SE increasing from 4.6 +/- 0.6 to 7.3 +/- 1.0%/min, p less than 0.02). Neither drug altered gastric acid secretion, but metoclopramide significantly increased gastric fluid output (mean +/- SE increased from 3.5 +/- 0.6 to 6.5 +/- 1.4 ml/min, p less than 0.02). No undesirable side effects or complications occurred during testing. We conclude that trials are warranted to assess the clinical efficacy of metoclopramide in infants with nonobstructive causes of delayed gastric emptying.

Bethanechol Compounds↗
PubMed1982

Effect of isoprenaline on bethanechol-stimulated gastric acid secrtion and mucosal blood flow in dogs with gastric fistula.

The prupose of this study was to elucidate the effect of the beta-adrenoceptor stimulation by isoprenaline on cholinergic-stimulated gastric acid secretion and mucosal blood flow in conscious dogs with gastric fistula. Isoprenaline, a beta 1- and beta 2-agonist, was used alone and in conjunction with selective blockade of beta 2 and beta 1 receptors. A low dose of isoprenaline had no significant effect, whereas higher doses had a significant antisecretory effect. The antisecretory effect was significantly blocked by the beta 1-adrenoceptor blocker practolol but not by H 35/25, a beta 2-adrenoceptor blocker. The dose-response curve with five doses of bethanechol with and without isoprenaline was in accordance with a non-competitive inhibition. There was no significant effect on gastric mucosal blood flow, indicating that the acid inhibition was not secondary to changes in blood flow. The inhibitory effect of isoprenaline seems to be mediated by the beta 1 receptors and with an action primarily on the 'gastrinergic receptors'.

Adrenergic beta-Antagonists↗
PubMed1980

Substance P, bethanechol, 4-aminopyridine, and potassium antagonize the depressing effects of low-frequency stimulation, tetrodotoxin, procaine, and of magnesium on the field-stimulated guinea-pig vas deferens.

The twitch-response enhancing potencies of (the agonists) substance P, bethanechol, 4-aminopyridine and of potassium chloride were compared in the field-stimulated guinea-pig vas deferens. The agonists were tested after the twitching activity of the isolated organ had been reduced to an equal extent by (the antagonists) tetrodotoxin, procaine, magnesium chloride, and by decreased stimulation frequency. Further experiments were performed in the functionally denervated organ. The potencies differed with the type of antagonism of the twitch-response. This pointed at different modes of action and/or sites of mechanism of the response-enhancing compounds. The pharmacological nature of agonists and antagonists as well as the results in the denervated organ indirectly suggested a predominantly neuronal point of mechanism of the agonists. This was most obvious for substance P.

4-Aminopyridine↗
PubMed1978

Urinary bladder smooth-muscle electrical activity: response to atropine and bethanechol.

Fourteen patients with spinal cord injuries and lower motor neuron type neurogenic bladders and 12 patients with upper motor neuron type neurogenic bladders and spinal cord injuries, were evaluated before and after bethanechol or atropine, respectively. They were compared with 5 patients with benign prostatic hypertrophy or bladder tumors but without neurologic disease. Both drugs were found to modify partially smooth-muscle response. The implications of these results are consistent with the production of electrical activity by the smooth-muscle cells of the bladder wall.

Atropine↗
PubMed1995

Use of bethanechol chloride to increase available ultrafiltration in CAPD.

Reabsorption of peritoneal dialysis fluid during the prolonged dwell time of continuous ambulatory peritoneal dialysis (CAPD) reduces the efficiency of ultrafiltration and sacrifices effective dialysis adequacy. Studies by Nolph indicate a predominant role of lymphatics in this fluid loss. Khanna has reported that lymphatic flow may be influenced by acetylcholine. This study was designed to determine if bethanechol chloride (BC) would increase the availability of drained volume during CAPD. Nine patients were studied, including 7 patients who exhibited inadequate ultrafiltration. During a 5-day control period, total dialysate drained volume was collected and a standard peritoneal equilibration test (PET) performed. This was followed by a corresponding 5-day test period in which BC (mean dose 0.27 +/- 0.13 mg/kg/day) was administered orally. Drained volume during the control standard 4-hr PET was 1996.68 +/- 279.87 mL. The result for the test period was 2363.33 +/- 321.13 mL (p < 0.05), indicating an 18.4% increase using BC. The PET indicated no change in transport of urea, creatinine, and glucose. In conclusion, the total drained volume can be effectively increased with a subsequent increase in metabolite clearance using BC. Patients exhibiting inadequate ultrafiltration were able to be maintained on CAPD using this cholinergic drug.

Absorption↗