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PubMed1980

Failure of the bethanechol supersensitivity test to predict improved voiding after subcutaneous bethanechol administration.

Subcutaneous administration of 5 mg. bethanechol chloride did not change significantly either flow rates or percentage residual urine in 11 patients with a positive bethanechol supersensitivity test. Therefore, a positive response to this test cannot be used to predict improved voiding function after subcutaneous or oral administration of the drug. Studies that purport to show a long-term rather than a short-term facilitory effect of this agent on voiding must satisfy rigid criteria, which include totally excluding a change in any other factor affecting the lower urinary tract.

Bethanechol Compounds↗

PubMed1989

Combined effect of disopyramide and bethanechol: use of bethanechol to prevent anticholinergic side effects of disopyramide without reduction of antiarrhythmic efficacy.

Because bethanechol chloride (B) relieves the anticholinergic side effects of disopyramide (D), we examined the combined effects of D and B on the heart and urinary bladder. B was confirmed to counteract dose dependently the effect of D on the dog bladder. In the ventricular muscle, the combined electrophysiological effects (D + B) were additive, with no reduction in the effect of D. With the control value set as 100%, the decrease in the maximum rate of depolarization with 5 X 10(-6) g/ml D (90 +/- 6%) was not affected by the same dose of B (D + B: 84 +/- 14%). Moreover, the effective refractory period (ERP) was larger with D + B (128 +/- 12%) than with either B (109 +/- 9%, p less than 0.01) or D (115 +/- 11%, p less than 0.05). In contrast, in the atrial muscle and AV and SA nodes, B had marked acetylcholine-like effects. These were completely suppressed by the addition of D except for the atrial ERP with the highest tested concentration of B (5 X 10(-6) g/ml). In the latter case, the prolongation of ERP was minimal (B + D: 105 +/- 14%) as compared with D alone (130 +/- 15%). Since the plasma concentration of B after oral administration of a clinical dose is expected to be on the order of 10(-7) g/ml, no practical effect is anticipated. We conclude that B can be expected to counteract urination disorders caused by D without reducing D's antiarrhythmic efficacy.

Anesthesia↗

PubMed1985

Bladder and urethral function and supersensitivity to subcutaneously administered bethanechol in cats with chronic cauda equina lesions.

The failure of bethanechol chloride to induce voiding in patients with neurogenic bladder, despite a positive bethanechol test, is being reported more frequently. An experimental model was designed in the cat to study the response of the bladder and urethra to subcutaneous and intraarterial bethanechol after complete and partial sacral decentralization. Complete sacral rhizotomy abolished the micturition reflex. Basal urethral perfusion pressure was not affected by complete sacral rhizotomy and a significant part of this basal urethral pressure remained sympathetically mediated. However, the urethral constriction response to bladder filling was lost in half the cats with complete lesions. Bladder and urethral supersensitivity to bethanechol chloride in cats with complete lesions was characterized by a shift to the left of the i.a. dose-response curve, and by the presence of responses to doses of s.c. bethanechol chloride which are subthreshold in normal cats. The urethra also showed exaggerated constriction responses to i.a. and s.c. bethanechol. After complete lesions a part of the bladder and urethral responses to s.c. bethanechol was adrenergically mediated and exerted through the vesicourethral short neuron system. The rest of the response was due to stimulation of urethral muscarinic receptors. Partial sacral lesions were compatible with a micturition reflex and the urethra retained its reflex response to bladder distension. After partial decentralization the bladder and urethra also showed responses to subthreshold doses of s.c. bethanechol. While the bladder response to s.c. bethanechol did not show a significant adrenergic component in cats with partial lesions, most of the urethral response was sympathetically mediated. In conclusion, complete cauda equina lesions result in an areflexic detrusor with frequent loss of the urethral responsiveness to bladder filling. Urethral supersensitivity to s.c. bethanechol might be responsible for a non-voiding outcome after bethanechol injection in patients with complete cauda equina lesions, despite a positive bethanechol test. Because the detrusor reflex is preserved and the urethra is less supersensitive to bethanechol after partial cauda equina lesions, these may represent a better indication for bethanechol therapy than do complete ones.

Animals↗

PubMed2000

Electromotive administration of intravesical bethanechol and the clinical impact on acontractile detrusor management: introduction of a new test.

PURPOSE: It is often difficult to determine the functional status of the detrusor muscle in patients with detrusor areflexia. We performed a clinical study to establish a test defining residual detrusor capacity in such patients. MATERIALS AND METHODS: In phase 1, 5 controls with detrusor areflexia were tested with an intravesical instillation of 20 mg. bethanechol in 150 cc of sodium chloride 0.3% with and without 20 mA. of pulsed current applied via an electrode catheter through the saline. Cystometry simultaneously recorded intravesical pressure changes. In phase 2, 45 patients with detrusor areflexia were tested with electromotive administration of intravesical bethanechol. In phase 3, 25 mg. bethanechol given orally once daily were prescribed for 15 patients and voiding control was assessed after 6 weeks of therapy. RESULTS: Neither bethanechol without current nor current through saline only led to increased intravesical pressure. However, we noted a mean pressure increase of 34 cm. water during the electromotive administration of bethanechol in 24 of 26 patients with areflexia and neurological disease compared to only 3 cm. water in 3 of 11 with a history of chronic bladder dilatation. Oral bethanechol restored spontaneous voiding in 9 of 11 patients who had had a positive response to the electromotive administration of bethanechol, whereas all 4 without a pressure increase during the electromotive administration of bethanechol did not void spontaneously. CONCLUSIONS: Electromotive administration of intravesical bethanechol identifies patients with an atonic bladder and adequate residual detrusor muscle function who are candidates for restorative measures, such as oral bethanechol and intravesical electrostimulation. Those who do not respond to the electromotive administration of bethanechol do not benefit from oral bethanechol and are candidates for catheterization.

Administration, Intravesical↗

PubMed1992

Bethanechol-induced responses in mudpuppy parasympathetic neurons.

The effect of bethanechol on membrane potential and excitability was determined in mudpuppy parasympathetic postganglionic neurons. Bethanechol induced a large amplitude hyperpolarization, which was followed by a smaller amplitude depolarization, in 115 out of 135 cells tested. In approximately 20% of these cells, a brief depolarization preceded the hyperpolarization. During the bethanechol-induced hyperpolarization, the membrane input resistance decreased markedly, whereas the input resistance was increased during the subsequent depolarization. The hyperpolarization and depolarization were blocked by atropine and were unaffected by d-tubocurarine, thus, both appeared to be mediated by muscarinic receptors. The bethanechol-induced hyperpolarization was inhibited by the M2 muscarinic receptor antagonist AF-DX 116, whereas the bethanechol-induced depolarization was unaffected. Both a nonselective increase in membrane conductance and a decrease in membrane potassium conductance appeared to be involved in the generation of the bethanechol-induced depolarization. Evidence for the first mechanism was obtained in barium-treated cells in which bethanechol initiated a rapid onset depolarization, which was reversed at membrane potentials near 0 mV. Evidence for the second mechanism was obtained when the hyperpolarization was inhibited by AF-DX 116. In AF-DX 116-treated cells, the membrane input resistance was increased during most of the bethanechol-induced depolarization. Mudpuppy neurons initiate repetitive action potential activity in response to long depolarizing current pulses. Following application of bethanechol, with the hyperpolarization negated electrotonically, the number of action potentials produced by a depolarizing current pulse was greater than that produced prior to application of bethanechol. It is suggested that activation of muscarinic receptors on mudpuppy cardiac neurons influences multiple conductance systems and determines the excitability of these neurons.

Animals↗

PubMed2004

Bethanechol provocation testing does not predict symptom relief after cholecystectomy for acalculous biliary pain.

BACKGROUND: The currently accepted hypothesis to explain acalculous gallbladder pain is the lack of contractile co-ordination between the body and neck. We have previously shown that bethanechol, a muscarinic stimulant causes differential stimulation of these two regions. AIM: To evaluate the reliability of bethanechol-induced gallbladder contraction in predicting symptom relief after cholecystectomy in patients with acalculous gallbladder disease. METHODS: Fifty-one patients underwent a bethanechol provocation test together with serial ultrasound to determine gallbladder emptying. McGill pain questionnaires were completed, and patients positive for pain (bethanechol provocation test +ve) were offered cholecystectomy, and patients negative for pain (bethanechol provocation test -ve) were reassessed at 6 months and offered cholecystectomy if symptoms persisted. All patients answered pain questionnaires either 6 months after surgery or as follow-up. RESULTS: There was no difference in the percentage of gallbladder emptying between the bethanechol provocation test +ve and bethanechol provocation test -ve groups. Fifty-three percent of bethanechol provocation test +ve patients and 54% of bethanechol provocation test -ve patients still remained symptomatic 6 months after surgery. Conclusion. Gallbladder pain provoked by bethanechol does not predict symptom relief after cholecystectomy.

Adult↗

PubMed2001

Effects of bethanechol on canine urinary bladder smooth muscle function.

We studied whether the effects of bethanechol are mediated via a muscarinic receptor, the role of extracellular calcium on bladder contraction, and down-regulation of bladder contraction by bethanechol after activation with potassium chloride (KCl) and acetylcholine (Ach). Smooth muscle strips of normal urinary bladder were studied with standard methods to measure isometric force. Bethanechol caused a dose-dependent increase in bladder contraction. The potency of bethanechol is higher than Ach, as shown by higher peak active isometric stress (P(max)) and lower half-maximal contraction (ED(50)) (P< 0.01). The contractile responses to bethanechol were diminished in the presence of atropine, nifedipine and in calcium-free medium as shown by P(max) decreased by 58%, 87% and 65% and ED(50) increased by 314-, 24- and 16-fold, respectively. When bladder strips were stimulated with KCl and Ach, pre-treatment with bethanechol reduced the responses to KCl by 116-242% (P<0.05), while the contractile responses to Ach were unaltered. Thus, bethanechol induces bladder contraction via muscarinic receptor activation while both intracellular and extracellular calcium play a crucial role on bladder smooth muscle contraction. The mechanisms of down-regulation by bethanechol may be related to interference with calcium influx into the smooth muscle cells, rather than the desensitisation of muscarinic receptors or post-receptor steps of signal transduction following bethanechol binding to the receptor.

Acetylcholine↗

PubMed1985

The effects of racemic bethanechol and its (R)- and (S)-enantiomers on pre- and postjunctional muscarine receptors in the guinea-pig ileum.

The effect of racemic bethanechol and its (R)- and (S)-enantiomers on smooth muscle contraction and outflow of [3H]-acetylcholine were studied in the guinea-pig myenteric plexus-longitudinal muscle preparation that had been preincubated with [3H]-choline. (S)-, racemic, and (R)-bethanechol caused concentration-dependent contractions of the longitudinal muscle. The potency ratio of the strong isomer (S) to the weak one (R) was 915. Racemic and (S)-bethanechol concentration-dependently inhibited the evoked outflow of [3H]-acetylcholine. Racemic bethanechol was more potent than (S)-bethanechol. (R)-bethanechol up to a concentration of 1 mM did no affect the evoked outflow of [3H]-acetylcholine. (S)-bethanechol was a substrate, and (R)-bethanechol a weak inhibitor of the tissue cholinesterases. The weak cholinesterase-inhibiting action of the (R)-enantiomer probably reinforces the prejunctional effects of the (S)-enantiomer in the racemic mixture.

Animals↗

PubMed2005

mu-Opiate receptor agonist loperamide blocks bethanechol-induced gallbladder contraction, despite higher cholecystokinin plasma levels in man.

UNLABELLED: mu-Opiate receptor agonists, such as loperamide, influence biliary excretion and suppress cholecystokinin (CCK)-induced gallbladder contraction. Loperamide decreases cholinergic mechanisms, like pancreatic polypeptide (PP) release, while muscarinic agonist (bethanechol)-induced PP release remains unaffected. The effects of loperamide on gallbladder contraction and peptide release were performed to resolve this discrepancy. METHODS: Six subjects (27.6 +/- 2.0 years) received bethanechol (12.5, 25 and 50 microg kg(-1) h(-1) continuously over 40 min) after oral 16 mg loperamide (vs placebo) in a crossover design. Gallbladder volume and plasma levels of CCK, PP, motilin, gastrin, neurotensin, cholylglycine were measured regularly. RESULTS: Bethanechol significantly reduced gallbladder volume (26.7 +/- 1.9 to a nadir of 15.3 +/- 2.2 mL, P < or = 0.05), and this action was inhibited by loperamide. Basal CCK levels increased significantly after loperamide. Incremental integrated CCK release after bethanechol was higher under loperamide (P < or = 0.05), as placebo CCK release was significantly decreased under bethanechol (2.0 +/- 0.4-0.8 +/- 0.3 pmol L(-1)). In both settings, PP levels were significantly increased after bethanechol, while release of neurotensin, motilin, gastrin and cholylglycine was unaffected. CONCLUSION: The mu-opiate receptor agonist loperamide inhibits bethanechol-induced gallbladder contraction. This effect is not mediated by inhibition of CCK release, as loperamide even enhances basal CCK plasma levels. As cholinergic mechanisms, like bethanechol-induced incremental PP release, were unaffected, mu-opiate agonists might influence gallbladder contraction via vagal-cholinergic pathways.

Adult↗

PubMed1992

Bethanechol inhibition of chicken intestinal brush border Na/H exchange: role of protein kinase C and other calcium-dependent processes.

Bethanechol, a muscarinic agonist, inhibits the initial rate of amiloride-sensitive Na uptake by intact mucosa of avian small intestine as well as by isolated chicken villus enterocytes, an effect that is maximal at 90 seconds and reverses by 6 minutes. Bethanechol similarly decreases intracellular pH in isolated cells suspended in bicarbonate-free buffer in a time course similar to inhibition of enterocyte Na uptake, suggesting inhibition of Na/H exchange. In brush border membrane vesicles rapidly prepared from cells stimulated with bethanechol, proton-dependent 22Na uptake is transiently inhibited in a time course similar to inhibition of cell Na uptake. Bethanechol also stimulates transient translocation of protein kinase C from the cytosol to the particulate fraction, a portion of this activity translocating to the brush border membrane. To determine the calcium dependence of bethanechol's action, enterocytes were loaded with varying concentrations of the calcium buffering agent quin-2. Inhibition of cell Na uptake by the calcium ionophore ionomycin could be completely reversed by quin-2 buffering in a concentration-dependent manner. In contrast, quin-2 buffering had little or no effect on the inhibition of Na uptake caused by the protein kinase C activators phorbol esters and oleoylacetylglycerol. Bethanechol's inhibitory effects were partially, but not completely reversed by quin-2 buffering. These data suggest that the effects of bethanechol on chicken villus enterocyte brush border Na/H exchange are mediated by calcium-dependent process(es) as well as by protein kinase C.

Animals↗

PubMed1982

Bethanechol-induced water intake in rats: possible mechanisms of induction.

Acute administration of the parasympathomimetic agent, bethanechol, at 2, 4, 8 and 12 mg/kg body wt, IP, induced drinking and increased urine output of rats in a dose-dependent fashion. The first significant increases in both water intake and urine output above that of controls occurred when 4 mg/kg was administered. The drinking and increased urine output in response to administration of 8 mg bethanechol/kg was inhibited by atropine sulfate (3 and 6 mg/kg, IP). In addition, the beta-adrenergic antagonist, propranolol (6 mg/kg, IP, administered 30 min prior to treatment with bethanechol), inhibited bethanechol (8 mg/kg, IP)-induced drinking. Urine output, however, was unaffected by propranolol. Further, the angiotensin I converting enzyme inhibitor, captopril, inhibited significantly the drinking response, but not the increased urine output, accompanying administration of bethanechol (8 mg/kg). The effect of bethanechol and the beta-adrenergic agonist, isoproterenol (25 micrograms/kg) separately and in combination, on water intake was also studied. Both compounds increased water intake but they exerted no interactive effect when administered simultaneously. Administration of bethanechol (8 mg/kg) to conscious rats was also accompanied by a significant reduction in both mean blood pressure and heart rate that reached minimal levels within 10 min after treatment. Both responses had returned to control level by one hr after treatment. These results suggest that bethanechol induces drinking in rats by way of the renin-angiotensin system.

Animals↗

PubMed1986

Bethanechol increases the diagnostic yield in patients with esophageal chest pain.

The diagnostic yield of routine esophageal manometrics in evaluating noncardiac chest pain is low. To determine if bethanechol stimulation would increase the diagnostic yield, we examined 87 patients with chest pain but no gastroesophageal reflux, 47 patients with gastroesophageal reflux but no chest pain, and 20 normal subjects. All subjects underwent standard esophageal manometrics before and after two doses of 50 micrograms/kg body wt bethanechol administered subcutaneously 15 min apart. Mean amplitude and duration of contractions and percentage of abnormal contractions were measured in the distal 7 cm of the esophageal body. Pathologic manometric parameters were defined as mean +/- 2 SD of values obtained in normal patients. Patients with chest pain had pathological responses for amplitude of contraction, duration of contraction, and percentage of abnormal contractions of 31%, 14%, and 22%, respectively, in the basal period. This increased to 43%, 66%, and 40%, respectively, after the first dose of bethanechol and to 53%, 85%, and 82% after the second dose of bethanechol. Chest pain was reproduced with new manometric abnormalities in 46% of patients after the first dose of bethanechol and in 77% after the second dose. Our conclusions are that: sequential bethanechol administration significantly increases the diagnostic yield of standard esophageal manometrics in the evaluation of noncardiac chest pain and duration of contraction after pharmacologic provocation with bethanechol is the best parameter to segregate patients with chest pain from normal subjects and gastroesophageal reflux patients.

Adult↗

PubMed1990

Central actions of bethanechol on the urinary bladder in dogs.

Bethanechol has been used to promote bladder emptying although the clinical efficacy of bethanechol remains uncertain. Both laboratory and clinical observations suggest that the pharmacologic actions of bethanechol are dependent to some extent on intact reflex mechanisms of the bladder. The objective of this study was to determine the effects of central nervous system administration of bethanechol on reflex detrusor contractions. Twelve isolated cross perfusion studies of the central nervous system in dogs were done to determine the cystometric response to central bethanechol administration. Central bethanechol resulted in reflex bladder contractions, decreased cystometric volume, increased maximum intravesical pressure, and increased periurethral EMG activity. This study demonstrated a central nervous system site of pharmacologic activity of bethanechol.

Animals↗

PubMed1994

Mechanisms for pancreatic hypertrophy induced by long-term administration of bethanechol.

Mechanisms for the hypertrophy of rat pancreas induced by long-term administration of bethanechol were investigated. The administration of bethanechol, an acetylcholine receptor agonist, to male Wistar rats for 14 days induced significant increases in the pancreatic weight and contents of protein, amylase and RNA in the pancreas without altering the content of DNA and the incorporation of [3H]thymidine into DNA. Simultaneous administration of atropine with bethanechol suppressed the bethanechol-induced pancreatic hypertrophy. Long-term administration of other acetylcholine receptor agonists also showed similar effects as produced by bethanechol. CR1505 (loxiglumide; D,L-4-(3,4-dichlorobenzoyl-amino)-5-(N-3-methoxypropyl-pentylam ino)-5- oxopentanoic acid), an antagonist of cholecystokinin receptors, inhibited pancreatic growth induced by long-term administation of pentagastrin, whereas pancreatic hypertrophy induced by bethanechol was not inhibited by CR1505. These results suggest that long-term administration of bethanechol induces pancreatic hypertrophy through direct activation of muscarinic receptors in the pancreas.

Amylases↗

PubMed2001

Involvement of potassium channels in spinal antinociceptions induced by fentanyl, clonidine and bethanechol in rats.

In the central nervous systems, intracellular and extracellular movement of potassium ions plays an important role in regulating neuronal excitability and the release of neurotransmitters. The purpose of our study was to determine whether nicorandil (adenosine triphosphate-sensitive K+ channel opener) exerts antinociceptive effects by itself or in combination with fentanyl, clonidine and bethanechol and whether glibenclamide (adenosine triphosphate-sensitive K+ channel blocker) and charybdotoxin (Ca2+-activated K+ channel blocker) may antagonize the antinociceptive action of fentanyl, clonidine and bethanechol. Antinociceptive effects were assessed using the tail-flick test in rats. Nicorandil (100 microg) and antinociceptively ineffective doses of fentanyl (1 microg), clonidine (2.5 microg) or bethanechol (10,ug) were coadministered intrathecally (i.t.). Glibenclamide (100 microg) or charybdotoxin (2.5 ng) were administered i.t. at 5 min before each effective dose of fentanyl (2.5 microg), clonidine (10 microg) or bethanechol (40 microg). The present findings demonstrated that i.t. administration of nicorandil alone exerted no influence on the tail-flick latency. However, concomitant administrations of antinociceptively inactive doses of fentanyl, clonidine or bethanechol with nicorandil elicited significant suppression of the thermonociceptive response. Also, each antinociception induced by fentanyl, clonidine or bethanechol was partially antagonized by both glibenclamide and charybdotoxin. These findings showed that activation of the K+ channel might enhance the antinociceptive effects of fentanyl, clonidine and bethanechol.

Adenosine Triphosphatases↗

PubMed1980

Response of the bladder to bethanechol after acute spinal cord transection in cats.

Immediately after spinal cord transection, normal bladder reflex activity is lost and voiding contractions in response to cholinergic drugs can no longer be elicited. Intravesical pressure responses to s.c. and i.a. bethanechol were studied in male cats before and after spinal cord transection at T6 to T7. Bethanechol s.c. enhanced spontaneous bladder activity and produced a sustained bladder contraction. The sustained response was abolished by spinal transection. The response of the bladder to i.a. bethanechol consisted of two phases. The first, dose-related phase, which resembled the response to i.a. acetylcholine, was unchanged by spinal cord transection, rhizotomy (L7-S3) or by ganglion blockade with hexamethonium. The second sustained phase, like the s.c. response, was markedly reduced by all three treatments. Because the response to bethanechol in vitro did not differ in control and transected preparations, it is unlikely that the depressant effects are due to a persistent change in bladder muscle responsiveness. No contractions were observed regardless of s.c. injection site; hence, altered drug absorption and distribution are not sufficient to explain the diminished responses observed. Because interruption of pelvic parasympathetic reflex pathways by rhizotomy and ganglion blockade interfered with the responses to s.c. and i.a. bethanechol, we conclude that bethanechol requires intact pelvic reflex pathways in order to produce sustained contractions. The prolonged action of bethanechol is an important feature contributing to its effectiveness. Removal of reflex functions by spinal cord transection might explain the ineffectiveness of cholinergic drugs in both patients and experimental animals in the acute, areflexic stage after spinal cord transection.

Acetylcholine↗

PubMed1989

Prospective evaluation of high-dose bethanechol in investigation of esophageal chest pain.

We compared the value of bethanechol 80 micrograms/kg subcutaneously, acid infusion with a 0.1 normal hydrochloric acid, and edrophonium 80 micrograms/kg intravenously as provocative agents to reproduce chest pain and manometric alterations in 72 patients with noncardiac chest pain. No patient developed typical chest pain and manometric alteration with acid infusion, while five (6.9%) patients developed these changes with edrophonium and four (5.6%) with bethanechol. Only one patient developed diagnostic changes exclusively with bethanechol. All patients tested with bethanechol developed some degree of local pain or significant cholinergic symptoms, with two patients requiring atropine for relief. Side effects from edrophonium were infrequent (28% of patients tested) and did not require atropine administration. We conclude that, using the parameters of typical chest pain and the development of manometric alterations as proof of the esophageal origin of chest pain, bethanechol at 80 micrograms/kg adds little information beyond that obtainable with edrophonium. Further, the high incidence of bethanechol-related side effects at 80 micrograms/kg suggests that this dose should not be generally recommended.

Bethanechol↗

PubMed1992

Galanin and bethanechol appear to activate the same inwardly rectifying potassium current in mudpuppy parasympathetic neurons.

Galanin- and bethanechol-activated whole cell currents were studied in dissociated mudpuppy parasympathetic neurons kept in 12.5 mM KCl. The bethanechol-induced current was reduced when generated during a galanin-induced current. The galanin and bethanechol currents reversed at -45 mV and exhibited inward rectification at more negative potentials. Both the galanin- and bethanechol-induced current relaxations recorded during negative voltage steps were fitted best by two exponentials with the averaged time constant values not significantly different for the galanin and bethanechol currents. We conclude that galanin and bethanechol activate a similar membrane potassium conductance which is different from the background potassium conductance.

Animals↗