Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bethanechol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1986

Early effects of bethanechol on the esophageal motor function of infants with gastroesophageal reflux.

Lower esophageal sphincter (LES) pressure, as well as esophageal peristaltic amplitude, duration, and velocity were measured in 16 infants with gastroesophageal reflux before administration of subcutaneous bethanechol, and at 10, 20, and 30 min after. Seven infants received 0.1 mg/kg, and 9 received 0.2 mg/kg. Significant increases in LES pressure occurred at both doses and lasted for 20 min. The amplitude and duration of peristaltic contractions were increased only after the larger bethanechol dose, and the increases were of greater magnitude in the distal esophagus than in the middle esophagus. The velocity of peristalsis decreased significantly in both the lower and middle esophagus, but only after the larger dose of bethanechol. Bethanechol had no effect on any motor function of the upper third of the esophagus. The changes in esophageal peristalsis produced by bethanechol may improve the efficiency of distal esophageal acid clearance and thus may be responsible in part for the therapeutic effect of bethanechol in infants with gastroesophageal reflux.

Bethanechol↗
PubMed1986

Effects of bethanechol on the pancreas in antrectomized and normal rats.

The effect of chronic administration of bethanechol and pentagastrin on the pancreas was examined. Rats were either antrectomized or subjected to a sham operation. Three weeks after surgery, rats received a daily intraperitoneal injection of either bethanechol (12 mg/kg) or pentagastrin (250 micrograms/kg) for 14 days. The fasting serum gastrin after bethanechol treatment increased to 1.89 times that of controls treated with saline. Although antrectomy decreased fasting serum gastrin to approximately 40% of controls, serum gastrin increased by 2.17 times that of the antrectomized rats and 1.37 times that of controls in the bethanechol group. After 14 days of bethanechol treatment, weight and amylase in the pancreas increased significantly compared with control; DNA and protein also increased 1.3 and 1.5 times that of control. The increase in DNA and pancreatic weight indicated that hyperplasia was the predominant mechanism. The pancreas showed atrophy in antrectomized rats but this was reversed by both bethanechol and pentagastrin. The results indicate that either endogenous gastric or extragastric gastrin release by cholinergic stimuli may have an important role in the regulation of pancreatic growth.

Animals↗
PubMed1987

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat.

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

Animals↗
PubMed1991

Effects of atropine on pancreatic response to bethanechol, cholecystokinin, and food intake in rats.

Atropine was used to examine the role of cholinergic mechanisms in the pancreatic secretory response to food intake. Unanesthetized rats with gastric, jugular vein, bile-pancreatic, and duodenal cannulas were used; bile-pancreatic juice was recirculated. The maximal response to bethanechol (4 mg.kg-1.h-1) was similar to cholecystokinin (CCK)-8-induced maximal secretion. Atropine (25-200 micrograms.kg-1.h-1) markedly inhibited basal amylase output and caused dose-related inhibition of the incremental response to a maximal dose of bethanechol. Atropine (50 micrograms.kg-1.h-1) shifted the dose-response curve to bethanechol (1-32 mg.kg-1.h-1) to the right but did not alter maximal amylase output. L 364718 (0.5 mg/kg), a CCK receptor antagonist, had no effect on bethanechol-stimulated pancreatic secretion. Atropine (50 micrograms.kg-1.h-1) did not affect the incremental responses to low doses of CCK-8; the maximal response occurred at a higher CCK-8 dose because atropine decreased basal secretion. Atropine (50 or 200 micrograms.kg-1.h-1) did not decrease the amylase response to ingestion of a liquid meal. We conclude that 1) bethanechol is a full agonist for stimulation of pancreatic enzyme secretion and its effects are not mediated by CCK release; 2) atropine is a competitive antagonist of bethanechol-induced pancreatic secretion in vivo but does not directly affect responses to CCK-8; 3) cholinergic mechanisms do not mediate the pancreatic enzyme response to a liquid meal in rats.

Animals↗
PubMed1990

Bethanechol induced contraction in mouse spleen.

Bethanechol was shown to induce contraction in mouse spleen. The possibility of initiating such response by stimulating solely muscarinic receptors was tested in isolated spleens from mice. The present data showed that bethanechol was able to further increase the maximum splenic contraction induced by phenylephrine, suggesting that the bethanechol induced contraction was possibly unrelated to stimulating adrenergic receptors. Moreover, clonidine which was able to suppress the phenylephrine induced splenic contraction, was unable to suppress the splenic contraction induced by bethanechol, and this result supported the above notion. These data suggest that the bethanechol induced splenic contraction could be the result of a direct stimulation of muscarinic receptors in mouse spleens, and an indirect effect mediated through the stimulation by bethanechol of sympathetic neurotransmitter release from sympathetic varicosities seems unlikely.

Animals↗
PubMed1986

Pirenzepine and propantheline effects on esophageal pressure responses to bethanechol.

Pirenzepine is an antisecretory anticholinergic type drug that has recently been shown to be relatively free of usual anticholinergic side effects on esophageal smooth muscle. It has also been suggested that this drug might release some of the inhibitory control of the esophagus and allow increased muscle contractions. To test this hypothesis, we compared the response of the lower esophageal sphincter (LES) and esophageal peristaltic contractions to bethanechol in 12 healthy controls after background oral doses of placebo, pirenzepine (50 mg), and propantheline (30 mg). After baseline placebo, bethanechol (40 micrograms/kg subcutaneously) produced the expected significant increases in LES pressure and amplitude of peristaltic contractions. Maximal increases were 51.9 +/- 14.9 and 29.5 +/- 7.0%, respectively. Also as expected, propantheline inhibited the cholinergic stimulation from bethanechol, allowing only a 10.1 +/- 13.6% increase in LES pressure and a decrease in peristaltic contraction amplitudes (-44.1 +/- 5.0%) after bethanechol. After background pirenzepine, the responses to bethanechol were intermediate between the other two drugs. A significant increase (44.2 +/- 16.4%) in LES pressure occurred after bethanechol while no significant changes (6.9 +/- 5.8%) were noted in peristaltic amplitudes with this drug. Typical side effects of dry mouth were noted in six of the 12 subjects with propantheline and in only three subjects after pirenzepine. These studies once again confirm the absence of usual anticholinergic side effects with oral pirenzepine compared to oral propantheline in the doses studied. We could find no evidence for a release of cholinergic inhibition after pirenzepine administration.

Adult↗
PubMed1984

Adrenergic influence on pentagastrin and bethanechol stimulated gastric acid secretion in dogs with gastric fistula.

The purpose of this study was to elucidate the effect of alpha-, beta- and dopaminergic receptor stimulation and blockade on pentagastrin and bethanechol stimulated gastric acid secretion in conscious dogs with gastric fistula. Gastric acid secretion was found to be subject to a dose related inhibition by isoprenaline. The dose of isoprenaline producing approximately 50% inhibition was higher in the bethanechol--than the pentagastrin experiments (0.10 vs. 0.03 micrograms/kg/min.) and slightly lower after parietal cell vagotomy. The antisecretory effect was mediated via the beta 1-receptors alone. The inhibitory effect of isoprenaline on pentagastrin stimulated acid secretion showed the characteristics of competitive type and on bethanechol stimulated acid secretion of non competitive type. An increasing and dose-dependent stimulation of bethanechol stimulated gastric acid secretion was found for dopamine 1, 5 and 10 micrograms/kg/min. Dopamine (40 micrograms/kg/min.) exerted an inhibitory effect on pentagastrin and bethanechol stimulated gastric acid secretion mediated, via the beta 1-receptors. The stimulatory effect of low doses of dopamine during bethanechol stimulation could not be defined as an effect via beta-receptors. This dual response, the weak inhibitory effects and the potent decreasing effect on antral gastric motility indicate that dopamine has no physiologic relevant effect on gastric acid secretion. One may conclude that beta 1- and beta 2-receptors may exert an influence on gastric acid secretion in dogs. The main effect of dopamine seems to be on gastric motility, while the effect on gastric acid secretion is of minor importance.

Adrenergic beta-Agonists↗
PubMed2000

Topical diltiazem and bethanechol decrease anal sphincter pressure and heal anal fissures without side effects.

PURPOSE: Topical glyceryl trinitrate heals anal fissures, but a majority of patients experience headache. Topical gels of the calcium channel blocker diltiazem and the cholinomimetic bethanechol significantly lower anal sphincter pressure in volunteers. This study investigated the use of these two new pharmacologic agents in the treatment of patients with chronic anal fissure. METHODS: Two studies were conducted, each involving 15 patients with chronic anal fissure. In each study patients underwent anal manometry and laser doppler flowmetry before treatment. They were treated with either 2 percent diltiazem gel or 0.1 percent bethanechol gel three times daily for eight weeks. Assessment every two weeks was by clinical examination, repeat anal manometry, and laser doppler flowmetry. Daily pain was assessed by linear analog charts. RESULTS: Fissures healed in 10 of 15 (67 percent) patients treated with 2 percent diltiazem gel and in 9 (60 percent) patients treated with 0.1 percent bethanechol gel. There was no significant difference in the pretreatment maximum resting sphincter pressure (MRP) between responders and nonresponders in either group. There was significant reduction in the pain score after treatment with diltiazem (P = 0.002) and bethanechol (P = 0.005) compared with that before treatment. MRP was significantly lower after diltiazem (P = 0.0001) and bethanechol (P = 0.02) compared with pretreatment MRP. No headaches or side effects were reported. CONCLUSIONS: Both topical diltiazem and bethanechol substantially reduce anal sphincter pressure and achieve fissure healing to a similar degree reported with topical nitrates, but without side effects.

Administration, Topical↗
PubMed2005

The effects of bethanechol and cisapride on urodynamic parameters in patients undergoing radical hysterectomy for cervical cancer. A randomized, double-blind, placebo-controlled study.

To evaluate the effects of bethanechol and cisapride on urodynamic parameters in patients undergoing radical hysterectomy for cervical cancer. In this double-blind, placebo-controlled study, 79 patients with cervical cancer were randomized to receive bethanechol (30 mg/day), cisapride (30 mg/day), bethanechol combined with cisapride (same doses) and placebo. Urodynamic study was performed, including flowmetry, cystometry, pressure-flow study and urethral pressure profile before radical hysterectomy. Medication was administered postoperatively during 30 days. At the end of this period, urodynamic evaluation was repeated. There was an increase in both the maximum cystometric capacity and bladder capacity at first desire to void in the placebo group compared to the other groups. The rate of detrusor instability was higher in the group that used bethanechol combined with cisapride. Detrusor pressure at maximum flow was significantly higher when cisapride was used. There was a significant increase in postvoid residual volume in the placebo group. In patients undergoing radical hysterectomy, bethanechol and cisapride determined lower cystometric capacity and decreased bladder capacity at first desire to void, a higher maximum flow rate and higher detrusor pressure at maximum flow, with lower postvoid residual volumes. The early use of bethanechol and cisapride after radical hysterectomies positively modified urodynamic parameters, determining a more efficient detrusor function.

Adult↗
PubMed2003

The cholinomimetic agent bethanechol activates IK(ACh) in feline atrial myocytes.

The effect of the cholinomimetic agent, bethanechol on macroscopic membrane currents was studied in dispersed cat atrial myocytes, using the whole-cell patch-clamp technique. Bethanechol activated an inward rectifying potassium current similar to I(K(ACh)), and a delayed rectifying-like outward current, similar to I(KM3) activated by pilocarpine, choline, and tetramethylammonium, and I(KM4) activated by 4-aminopyridine. The relatively specific muscarinic receptors subtype antagonists methoctramine (M(2)), and tropicamide (M(4)) inhibited both current components induced by bethanechol, suggesting a lack of specificity of these antagonists on cat atrial myocytes. The specific antagonist of M(3) receptors, para-fluoro-hexahydro-siladifenidol did not significantly inhibit the bethanechol-induced currents. In addition, pretreatment with PTX prevented activation of the bethanechol-induced inward and outward currents, suggesting that M(3) receptors are probably not involved in the bethanechol action. The I(K(ACh)) specific blocker tertiapin inhibited both inward rectifying- and delayed rectifying-like currents. These results suggest that both current components result from activation of a single channel type, likely I(K(ACh)).

Animals↗
PubMedDate not supplied

Bethanechol for pediatric gastroesophageal reflux: a prospective, blind, controlled study.

To investigate the effect of bethanechol on postprandial gastroesophageal reflux in children, and the relationship between its effect on the lower esophageal sphincter pressure and its effect on reflux, we studied 31 consecutive children with pathologic reflux, using manometry and pH probe, both before and after administration of bethanechol. The initial sphincter pressure was subnormal in only 35% of the patients. The bethanechol-treated sphincter pressure was increased in 97% of the patients (from 13.4 +/- 1.3 to 34.1 +/- 2.6 mm Hg) and was normal in 97% of the patients, yet bethanechol did not improve any measure of postprandial reflux in the patient group as a whole. Furthermore, the 20 patients with normal sphincter pressures had significant worsening of their percent of postprandial time with reflux (from 21.8 +/- 5.3 to 33.8 +/- 6.0%, p = 0.009). Thus, this study demonstrates a failure of the acute administration of bethanechol to improve postprandial gastroesophageal reflux and raises the issue of whether the widespread use of bethanechol to treat reflux in children is appropriate.

Bethanechol Compounds↗
PubMed2001

Does bladder tone influence sensation of filling and electro-sensation in the bladder? A blind controlled study in young healthy volunteers using bethanechol.

PURPOSE: The influence of bladder tone on filling sensation and electro-sensation in the bladder was studied in young healthy volunteers. MATERIALS AND METHODS: A total of 22 healthy volunteers 18 to 30 years old were included in our study, of whom 15 received a subcutaneous injection of 5 mg bethanechol and 7 received a subcutaneous injection of water to serve as randomly selected controls. In each group filling perception was evaluated during medium fill cystometry before and 25 minutes after injection. The bladder electrical threshold was determined in each group by constant current stimulation before and 25 minutes after injection. RESULTS: In the study group there was a marked decrease in the volume at which various filling sensations occurred after bethanechol was given. The pressure at which all filling sensations were perceived was higher after bethanechol than at baseline cystometry. The electrical threshold decreased with bethanechol. In the control group no change was noted in the perception of filling or electro-sensation. CONCLUSIONS: Bethanechol has a distinct influence on the filling sensation and on electrical bladder stimulation. Each sensation is sharpened after the administration of bethanechol. Several hypotheses are possible to explain these effects.

Adolescent↗
PubMed1995

Effect of bethanechol, neostigmine, metoclopramide, and propranolol on myoelectric activity of the ileocecocolic area in cows.

The effect of bethanechol, neostigmine, metoclopramide, and propranolol on myoelectric activity of the ileum, cecum, and proximal loop of the ascending colon was determined in 6 healthy Jersey cows implanted with 8 pairs of bipolar electrodes. Assigned at random, each cow received each of 5 treatments in 3-day intervals. The treatments included bethanechol (0.07 mg/kg of body weight, SC), neostigmine (0.02 mg/kg, SC), metoclopramide (0.15 mg/kg, IM), DL-propranolol (0.2 mg/kg, IM), and 0.9% sodium chloride (NaCl) solution (20 ml, SC). All drugs were administered during early phase I of the migrating myoelectric complex in the ileum. Myoelectric activity was recorded for 4 hours after treatment, and data were analyzed for each hour separately. Bethanechol and neostigmine significantly (P < 0.05) increased the number of cecocolic spikes per minute per electrode, duration of cecocolic spike activity (%), and number of cecocolic propagated spike sequences per 10 minutes, relative to NaCl, during 1 or more hours of the recording period. The effect of bethanechol was more pronounced on duration of spike activity and number of propagated spike sequences, whereas neostigmine mainly increased the number of (uncoordinated) spikes. Metoclopramide and propranolol had no significant effect on cecocolic myoelectric activity, relative to NaCl. It was concluded that bethanechol and, less likely, neostigmine at the dosage used in this study may be suitable for medical treatment of cecal dilatation in cattle in which hypomotility of the cecum and proximal loop of the ascending colon has to be reversed. The potential advantage of bethanechol vs neostigmine for medical treatment of cecal dilatation is worth further evaluation.

Adrenergic beta-Antagonists↗
PubMed1996

Effect of bethanechol or erythromycin on gastric emptying in horses.

OBJECTIVE: To investigate the prokinetic effect of bethanechol and erythromycin in the upper gastrointestinal tract of healthy horses by measuring the gastric emptying (GE) rate of a radioactive meal. ANIMALS: 4 healthy adult horses. PROCEDURE: After food was withheld for 12 hours, horses were given 370 MBq of 99mTc-labeled sulfur colloid incorporated into egg albumen and 37 MBq of 111In-labeled diethyltriaminepentaacetic acid in 120 ml of water via nasogastric intubation. Intravenously administered treatments were 0.9% NaCl solution, erythromycin (0.1 or 1.0 mg/kg of body weight), or bethanechol (0.25 mg/kg). All drugs were given in 10 ml of 0.9% NaCl solution. Dual-phase scintigraphic images were obtained by use of a gamma camera. The best-fit function was determined for each study, and the resultant curves were then analyzed by use of least squares nonlinear regression. Two variables, time to 50% emptying of the stomach (T-50) and slope of the emptying curve, were derived from the calculated power exponential equation. CONCLUSIONS: Treatment had a significant (P < 0.05) overall effect on T-50 of solid-phase GE. The T-50 of bethanechol (30.09 +/- 10.01 minutes), erythromycin at 0.1 mg/kg (59.08 +/- 10.01 minutes), and erythromycin at 1 mg/kg (60.50 +/- 10.01 minutes) were significantly shorter than T-50 after saline administration (89.97 +/- 10.01 minutes). There was a trend (P = 0.09) for the slope of solid-phase GE of bethanechol and erythromycin (0.1 mg/ kg; P = 0.37) to be steeper than that of saline solution. For liquid-phase GE, the T-50 and the slope of bethanechol differed significantly (P < or = 0.05) from those for saline solution. CLINICAL RELEVANCE: Bethanechol and erythromycin significantly increased solid-phase GE in healthy horses and may have value for use as prokinetic agents in certain gastrointestinal tract diseases.

Animals↗
PubMed1993

Effects of subcutaneous bethanechol on bladder sensation during cystometry.

Bethanechol has been shown to produce a pharmacologic effect on the urinary bladder, although the clinical efficacy of this response is controversial. The measured response has been an increase in detrusor pressure, although sensory effects may occur also. In this study, 10 neurologically intact men had cystometry before subcutaneous administration of 5 mg bethanechol chloride and thirty minutes after bethanechol. The sensation of desire to void and the maximum cystometric capacity occurred at a higher intravesical pressure and a smaller bladder capacity following bethanechol. Subcutaneous bethanechol appears to alter the bladder pressure and capacity at which the perception of desire to void and the sensation of maximum fullness occurs.

Aged↗
PubMed1985

Effect of acute selective sacral rhizotomy in cats on bladder and urethral function and the response to bethanechol chloride.

Bladder and urethral responses to filling and to subcutaneous bethanechol are dependent upon intact sacral innervation. Acute selective sectioning of nerve roots in chloralose anesthetized cats was used to compare the sacral innervation requirements for the support of these responses. The detrusor was found to require primarily intact S2 roots although an S2 root on one side could, alone, subserve a weak, unsustained detrusor reflex. The urethral reaction to bladder filling required an afferent sacral pathway through either S1 or S2 roots. The sustained bladder response to subcutaneous bethanechol required greater sacral innervation than the detrusor reflex inasmuch as the S2 segment could subserve this response in only half the cases, and unilateral rhizotomy L7-S3 eliminated the response in half the cases. Both treatments, however, were compatible with a preserved detrusor reflex. The urethral constriction response to subcutaneous bethanechol required an intact sacral afferent pathway through either the S1 or S2 segments. In conclusion, the detrusor and urethral reflex responses to bladder filling and subcutaneous bethanechol require a certain amount of intact sacral innervation through S1 and S2 which is least for the detrusor reflex and greatest for the bladder response to subcutaneous bethanechol.

Animals↗
PubMed1984

Urethral response during bladder contraction induced by subcutaneous bethanechol chloride: elicitation of a sympathetic reflex urethral constriction.

The responses of the urethra to bladder filling and to subcutaneous bethanechol were studied in a surgically separated bladder-urethra preparation in chloralose anesthetized cats. With the pudendal nerves cut or the neuromuscular junction blocked with gallamine, urethral closure pressure increased during bladder filling and the initial phase of the micturition contraction. It then fell spontaneously or in response to bladder emptying through a vent. With the bladder volume held constant subcutaneous bethanechol induced an increase in basal bladder pressure which culminated in a sustained (reflex) contraction. The urethral constrictor response resembled that seen during the cystometrogram; an increase during the rise in detrusor pressure and a fall during the latter part of the sustained (reflex) contraction. In both cases the urethral response was substantially depressed by hypogastric nerve transection or by intravenous prazosin, implying that the urethral responses were reflexly mediated through the sympathetic system. Intra-arterial bethanechol also produced a urethral constriction, but this response was abolished by atropine and not affected by hypogastric nerve section or prazosin. It is therefore concluded that although bethanechol can produce urethral constriction through a direct muscarinic action on the urethra, it does not do so after subcutaneous administration in a neurally intact cat. The urethral response seen after subcutaneous bethanechol administration is part of the micturition reflex complex and is sympathetically mediated.

Animals↗
PubMed1991

Modulation of gastric contractions in response to tachykinins and bethanechol by extrinsic nerves.

1. Extrinsic reflexes elicited by changes in gastric wall tension play an important role in regulating gastric tone. The present study investigated whether such reflexes modulate gastric contractions induced by close arterially administered neurokinin A (NKA), substance P (SP), SP-methylester and bethancehol in anaesthetized rats. 2. Reflex pathways were acutely interrupted by either subdiaphragmatic vagotomy or prevertebral ganglionectomy. C-fibre afferent nerve activity was abolished by pretreating rats with capsaicin 10 to 16 days before the experiments. 3. The order of potency in inducing gastric contractions was NKA greater than SP greater than bethanechol. SP-methylester was markedly less effective than SP and its effects did not fit sigmoid dose-response curves (DRCs). The maximal responses to NKA, SP, and bethanechol were similar, whilst the DRC for SP was significantly flatter than those for NKA or bethanechol. Pretreatment of the rats with the peptidase inhibitors phosphoramidon or captopril did not increase the contractile response to SP. 4. Prevertebral ganglionectomy had no significant effect on the DRCs for SP and NKA, whereas vagotomy shifted the DRCs for all three test substances to the left. 5. Capsaicin pretreatment did not change the DRC for NKA in rats with intact vagus but shifted that for bethanechol to the left. The leftward of the DRC for NKA caused by vagotomy was prevented in capsaicin-pretreated rats whereas the vagotomy-induced shift of the DRC for bethanechol remained unaltered. The shift of the DRC for SP seen in response to vagotomy was only slightly reduced by capsaicin pretreatment. 6. These data may be interpreted as demonstrating two neuronal mechanisms for modulating drug-induced gastric contractions. First, the contractions themselves activate a vago-vagal negative feedback involving capsaicin-sensitive afferents. Second, NKA, and to a lesser degree SP, seem to induce a nonvagal non-splanchnic mechanism which via capsaicin-sensitive afferent neurones reinforces tachykinininduced gastric contractions.

Animals↗