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PubMedDate not supplied

Proton magnetic resonance spectroscopic determination of bethanechol chloride in tablets.

A simple and reliable proton magnetic resonance spectroscopic method was developed for the assay of bethanechol chloride in tablets. The proposed method entails a minimum of procedural steps and reagents. The recovery of bethanechol chloride from synthetic formulations was 99.9 +/- 0.4% (n = 15), CV = 0.4%. Mean assay values for 25 and 10 mg commercial tablets were 100.5% (n = 8) and 99.7% (n = 7) of declared, respectively. A detailed interpretation of the proton magnetic resonance spectrum is also presented.

Bethanechol↗
PubMed1987

Exocrine pancreatic response to secretin and bethanechol in rabbits under hypothermia.

The effect of the administration of secretin and bethanechol on exocrine pancreatic secretion was studied in rabbits subjected to temperature changes; these involved a drop from 38 degrees C +/- 1 to 28 degrees C +/- 1 (hypothermia) and a subsequent return to 38 degrees C +/- 1 (normothermia). It was observed that hypothermia does not depress the action of secretin on the secretion of fluid, HCO3- and Cl-. Neither was the action of bethanechol on the enzyme secretion affected by changes in body temperature.

Animals↗
PubMed1993

Bethanechol in the treatment of stuttering.

A double-blind trial of bethanechol for the treatment of stuttering that used a crossover experimental design failed to find the drug superior to placebo. However, two of the patients who did respond favorably elected to continue with the medication and have remained more fluent after taking the drug for 6 months. The notion of "bethanechol responders" is advanced.

Adult↗
PubMed1989

Effect of metoclopramide, bethanechol, and loperamide on gastric residence time, gastric emptying, and mouth-to-cecum transit time.

The effects of metoclopramide, bethanechol, and loperamide on the gastric residence time (GRT), gastric emptying (GE), and mouth-to-cecum transit time (MCTT) of a solution were investigated in three separate studies of five healthy male volunteers each. Metoclopramide in doses of 5, 10, and 15 mg prolonged GRT by 33, 88, and 162%, respectively, almost reaching statistical significance (p 0.058). A relationship was observed between GRT prolongation, and metoclopramide area under the plasma-time curve (p 0.01) and metoclopramide observed time to maximum concentration (p 0.01). Metoclopramide had an inconsistent effect on MCTT. Bethanechol 50 mg prolonged GRT by 64% (p 0.031) and had no effect on MCTT. Loperamide at doses of 2 and 8 mg prolonged GRT by 18 and 115% (p 0.043) and MCTT by 30 and 130% (p 0.0001), respectively. None of these motility-altering agents affected GE.

Adolescent↗
PubMed1978

Responses of the rat superior cervical ganglion in vitro to isoprenaline and bethanechol.

The effects of isoprenaline were studied in isolated rat superior cervical ganglia. Intracellularly recorded excitatory postsynaptic potentials were depressed by isoprenaline in concentrations of 10(-5) to 10(-4)M. In 13 out of 17 cells, isoprenaline caused ganglionic hyperpolarization (mean, 4mV). Changes in the amplitude and contour of antidromic action potentials caused by isoprenaline could be accounted for by the increased membrane potential. A slight increase in membrane input resistance from 44--50.2 megohms (mean values) occurred in about half of the cells. Activation of an ion pump by isoprenaline was suggested by the finding that the hyperpolarization did not occur when the bathing solution contained ouabain (10(-5)M) or lacked Na+ or K+. Characterization of the isoprenaline effects by the use of alpha and beta adrenergic blocking drugs was not possible because of the direct depressant effects of the antagonists. The muscarinic agonist bethanechol (2.5 X 10(-5) to 2.5 X 10(-4)M) caused ganglionic depolarization and increased input membrane resistance (42--52 megohms) during depolarization in each of the cells tested. The ganglionic responses to bethanechol were prevented by atropine.

Action Potentials↗
PubMed1981

Effect of oral bethanechol on parameters of esophageal peristalsis.

It has been suggested that enhanced esophageal peristalsis may be an additional reason for the therapeutic effect of oral bethanechol (B) in reflux patients and for the improved acid clearing seen with B. This study was designed to determine the effect of oral B on various parameters of esophageal peristalsis. Healthy young adult males were studied with an intraesophageal transducer assembly. Amplitude, dp/dt, and velocity profiles for the smooth muscle portion of the esophagus were produced. Oral B, 25 mg, produced a significant increase (P less than 0.05) in amplitude in the distal esophagus from 15 to 45 min after drug administration. The effect on dp/dt was similar but not as marked. Oral bethanechol produced decreases in velocity at all points, reaching significance (P less than 0.05) at the most distal measuring site, 30 and 45 min after injection. Oral B produces a stronger but slower, perhaps more efficient, progression of the peristaltic wave in normal humans. Our findings may explain improved acid clearance found with this agent.

Adult↗
PubMed1981

The effect of ranitidine on gastric acid secretory response curves to histamine, pentagastrin or bethanechol in the dog with a Heidenhain pouch.

The H2-receptor antagonists ranitidine and cimetidine were tested against gastric secretory dose-response curves to histamine, pentagastrin and bethanechol in the Heidenhain-pouch dog. Histamine-induced gastric secretion was antagonized in a competitive manner by both ranitidine and cimetidine, but ranitidine was approximately 8 times more potent than cimetidine. Pentagastrin -induced secretion was markedly reduced by ranitidine and cimetidine but this antagonism was not competitive in nature. Bethanechol-induced gastric secretion was slightly reduced by both drugs. These findings are discussed in relation to the physiological control of gastric secretion.

Animals↗
PubMed1977

Action of oral and parenteral bethanechol on decompensated bladder.

A double blind balanced Latin-square study was conducted on 20 adult patients with decompensated bladders to determine the relative effectiveness of oral and parenteral bethanechol chloride (Urecholine) on the stretch response of bladder muscle. Detrusor reaction was measured by modified cystometry. Five mg. of subcutaneous bethanechol chloride produced a significant increase in intravesical pressure which was more rapid in onset, of larger magnitude, and of shorter duration than oral doses of 100 and 200 mg.

Administration, Oral↗
PubMed1980

Use of bethanechol for the treatment of gastroesophageal reflux.

A double-blind crossover study utilizing bethanechol was performed among 45 pediatric-aged patients with gastroesophageal reflux. Thirty young children (age = less than 1 year) were studied. These infants did significantly better while taking bethanecol than when they were receiving placebo. Fifteen children (age greater than 1 year) were also studied. These patients also had significant clinical improvement while on the drug when compared to the period when they were receiving placebo. Esophageal pH probe testing after the oral administration of bethanecol showed a significant decrease in frequency and duration of episodes of gastroesophageal reflux. This improvement may be secondary to the increases in lower esophageal sphincter pressure and persistaltic activity seen during esophageal manometrics. Bethanechol should be considered for pediatric-aged patients who are not benefited by conventional medical therapeutic regimens.

Adolescent↗
PubMed1998

Bethanechol activates a post-receptor negative feedback mechanism in rabbit urinary bladder smooth muscle.

PURPOSE: Recent studies using vascular and gut smooth muscles indicate that contractile receptor agonists may activate post-receptor down-regulatory mechanisms causing a temporary reduction in the strength of subsequent contractions. Our data indicate a similar mechanism exists in detrusor smooth muscle of the urinary bladder. MATERIALS AND METHODS: Each isolated strip of female rabbit detrusor was placed in a tissue bath, secured to an isometric force transducer, and length-adjusted until depolarization with 110 mM KCl produced a maximum contraction (S0). Subsequent contractions were normalized to S0 (S/S0) or to a first stimulus with 30 mM KCl or caffeine (S/S1). Tissues were pretreated with the muscarinic receptor agonist, bethanechol (BE), then stimulated with KCl, caffeine, or Bay k 8644 to identify potential post-receptor down-regulation. RESULTS: Contractions induced by 30 mM KCl had three phases labeled fast peak (FP), slow peak (SP) and steady-state (SS). In tissues exposed for 30 min. to a maximum BE concentration then washed for 5 min., the KCl-induced FP and SP, but not SS, responses were reduced by approximately 40%. Smaller reductions in peak KCl-induced contractions occurred in tissues pretreated for a shorter duration or with a 100-fold lower BE concentration. This down-regulation induced by bethanechol pretreatment was reversible, lasting approximately 1-2 h. Not only were KCl-induced contractions reduced by BE pretreatment, but also those produced by the intracellular Ca(2+)-mobilizer, caffeine, and the L-type Ca2+ channel agonist, Bay k 8644. CONCLUSIONS: Pretreatment of isolated strips of rabbit detrusor with a muscarinic receptor agonist produced short-term down-regulation of KCl-induced peak contractions that may have involved inhibition of both influx of extracellular Ca2+ and release of intracellular Ca2+. Reductions in the degree of this novel modulatory response during disease conditions and aging could enhance contractile activity, possibly causing detrusor instability.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1980

Positive bethanechol chloride supersensitivity test in hereditary sensory neuropathy.

An 11-year-old girl with hereditary sensory neuropathy (type II) presented with neurogenic bladder disease. Urodynamic evaluation revealed a sensory neurogenic bladder and a markedly positive bethanechol chloride supersensitivity test. This case report supports Lapides' original observation that a positive bethanechol chloride supersensitivity test may occur in pure sensory neurogenic bladder disease.

Bethanechol Compounds↗
PubMed1980

Failure of bethanechol denervation supersensitivity as a diagnostic aid.

A total of 33 patients who demonstrated detrusor areflexia during cystometry underwent the bethanechol denervation supersensitivity test. In each instance the presence or absence of a neurologic lesion was documented carefully by complete neurologic evaluation. Of the 21 patients with a neurogenic bladder there was a falsely negative rate of 24 per cent. Of the 12 patients without a neurogenic bladder the falsely positive rate was 50 per cent. It is concluded that a positive bethanechol test is not by itself indicative of neurogenic bladder nor does a negative test exclude this diagnosis.

Adult↗
PubMed1979

Malacoplakia of the bladder: efficacy of bethanechol chloride therapy.

Present evidence suggests that malacoplakia is the result of a functional defect in the mononuclear cells of the lesion caused by a deficiency of cyclic 3',5' guanosine monophosphate. This defect results in the impaired ability of the macrophage to release lysosomal enzymes necessary for the digestion of phagocytized bacteria. The persistent inflammatory reaction produces the characteristic granuloma of malacoplakia. Previous laboratory studies indicate that the phagocytic defect is reversible by cholinergic agonists, which led to the use of bethanechol chloride in the treatment of patients with malacoplakia. We report on 3 patients with vesical malacoplakia who were treated successfully with bethanechol chloride.

Adult↗
PubMed1977

Diabetic visceral neuropathy: treatment with bethanechol chloride.

An 86-year-old diabetic man developed nausea, emesis, abdominal distention, and decreased gastrointestinal motility. A Hollander test confirmed incomplete vagal dysfunction. Treatment with bethanechol chloride resulted in marked improvement which was reproducible after withdrawal and reinstitution of therapy. We believe that treatment with bethanechol chloride deserves further investigation in selected patients with diabetic visceral neuropathy.

Aged↗
PubMed1994

Electrophoretic analysis of cat parotid saliva in response to parasympathetic stimulation or infusion of bethanechol.

The protein constituents of cat parotid saliva evoked by parasympathetic stimulation or the infusion of bethanechol have been compared by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). The SDS-PAGE patterns were highly reproducible for an individual cat and revealed up to 30 polypeptide bands in microlitre volumes of unconcentrated saliva. Only minor and predominantly quantitative differences were detected in the salivary protein composition of different cats. SDS-PAGE demonstrates quantitative rather than qualitative changes in the protein composition of saliva evoked in response to different stimuli. The latter included preliminary observations on the effect of vasoactive intestinal peptide (VIP) on the bethanechol-evoked response.

Animals↗
PubMed2006

M3 muscarinic receptor-deficient mice retain bethanechol-mediated intestinal ion transport and are more sensitive to colitis.

Acetylcholine (ACh) is an important regulator of intestinal epithelial ion transport via muscarinic or nicotinic ACh receptors. Previous studies emphasize the role of the M3 muscarinic receptor subtype in mediating the effects of cholinergic agonists on intestinal ion transport. With the prevalence of mouse models to study intestinal (patho)physiology, it is crucial that ion transport be understood in this species. Using M3 receptor-deficient (KO) mice and wild-type (WT) mice, we examined M3 receptor contributions to ion transport as well as its role in colitis induced by dextran sodium sulphate (DSS). In the Ussing chambers, ileal and colonic tissue from M3 KO and WT mice displayed similar baseline ion transport properties. Short-circuit current (ISC) responses to the muscarinic receptor agonist bethanechol were slightly decreased in ileal tissue from M3 KO mice compared with tissue from WT mice, whereas responses were not significantly different in colonic tissue. ISC responses to bethanechol were partially inhibited by pirenzepine in WT ileum, but not tetrodotoxin, suggesting involvement of a non-neuronal M1 muscarinic receptor. In the ileum, the M3 receptor may inhibit neuronally evoked ion transport, as indicated by the increased ISC responses to electrical stimulation in tissue from M3 KO mice. Furthermore, whereas all DSS-treated mice developed colitis, M3 KO mice displayed more rapid mass loss and more severe disease than DSS-treated WT mice, even following a reduction in the amount and time of DSS treatment. Thus, M3 receptor-KO mice are compensated in their ability to evoke muscarinic receptor-driven ion transport responses, but are more sensitive to DSS. This work highlights the need to dissect muscarinic receptor-mediated events in the mouse, as mice become increasingly valuable in enteric disease models.

Animals↗