Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bethanechol Compounds”

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 631 records · Page 35Linked to original sources
PubMed1970

Relationship between pancreatic secretion and pancreatic blood flow.

An indicator fractionation technique using radioactive rubidium has been used to measure pancreatic blood flow after infusions of secretin, pancreozymin, urecholine, and pentagastrin. Secretin resulted in the production of a large volume of low viscous pancreatic juice and was associated with an increase in the cardiac output. Duodenal and pancreatic blood flow and perfusion rate were increased significantly. Blood flow to the remainder of the gastrointestinal organs was only marginally increased but the perfusion rate in each organ was increased significantly.Infusion of pancreozymin, urecholine, and pentagastrin resulted in the output of a small volume of viscous juice and was associated with no increase in cardiac output but with an increase in both pancreatic blood flow and perfusion rate.

Animals↗
PubMed1982

Effects of fundic vagotomy and cholinergic replacement on pentagastrin dose responsive gastric acid and pepsin secretion in man.

The effects of fundic vagotomy on acid and pepsin secretion in 12 patients (10 males, two females; nine duodenal ulcer, three gastric ulcer) were studied using a pentagastrin dose response before and after Vagotomy. In the intact stage H, Cl, and pepsin output all had the same ED50, 120-127 pmol/kg/h. Vagotomy reduced basal output of acid by 78%, Cl- by 50%, and pepsin by 62%. Postvagotomy basal outputs were not related to preoperative levels, while maximum acid output was reduced by an average of 35%, proportionally to the preoperative output (r = 0.94). Vagotomy uncompetitively (ED50 increase, Vmax decrease) inhibited the pentagastrin dose response of acid, chloride, and pepsin output. Postoperatively, a six-fold greater dose of pentagastrin (450 vs 76 pmol/kg/h) was required to stimulate acid to 50% of its preoperative maximum output. For pepsin secretion the increase was 12-fold (185 vs 15 pmol/kg/h). In five of the nine duodenal ulcer patients pentagastrin dose responses were repeated with a background infusion of urecholine, 20 micrograms/kg/h. Urecholine increased basal and peak acid, pepsin, and chloride outputs, and the ratio of basal: maximal almost to prevagotomy levels; it also restored the sensitivity to pentagastrin. Serum gastrin was not significantly changed by urecholine or by vagotomy. We conclude that the level of basal acid and pepsin secretion in ulcer patients, which is largely eliminated by vagotomy, is dependent on the vagus and not on serum gastrin. The effects of vagotomy are functional, are due to cholinergic withdrawal, and usually can be restored by cholinergic replacement.

Adult↗
PubMed1985

Calcitonin gene related peptide inhibits basal, pentagastrin, histamine, and bethanecol stimulated gastric acid secretion.

This study was designed to examine the effect of calcitonin gene related peptide on gastric acid secretion in the rat. Calcitonin gene related peptide (1 pmol-1 nmol/rat) injected intravenously inhibited basal gastric acid secretion in awake, freely moving rats. Calcitonin gene related peptide decreased gastric secretion stimulated by histamine, pentagastrin, or bethanecol in anaesthetised rats. The inhibitory effect was immediate and most pronounced in the first hour and diminished during the second hour. The N- and C-terminal fragments of calcitonin gene related peptide, CGRP1-14 and [Tyr23]CGRP23-37, did not affect gastric acid secretion. [acetamidomethyl-cys2,7]CGRP, the linear cysteine-protected molecule devoid of the disulphide bridge, was not biologically active. After truncal vagotomy or atropine sulphate, calcitonin gene related peptide did not inhibit gastric secretion. These studies indicate that calcitonin gene related peptide administered peripherally inhibits basal and stimulated gastric acid secretion in the rat. Both C- and N-terminal residues as well as the disulphide bridge are necessary for the inhibitory effect on gastric secretion. Inhibition of gastric acid secretion by calcitonin gene related peptide may depend on intact vagal cholinergic fibres.

Animals↗
PubMed1985

Prevention of duodenal ulcers in the rat using a combination of ranitidine and sucralphate in subtherapeutic doses.

This study investigated whether ulcer prevention would be greater with the combined use of an acid-inhibiting agent, ranitidine, given together with a mucosal-protective agent, sucralphate. Duodenal ulcers were induced in rats with the secretagogues pentagastrin and bethanechol. Subtherapeutic doses of ranitidine (5 mg/kg/6 hours) and sucralphate (50 mg/6 hour) yielded an ulcer index of 4.0 and 4.1 respectively, not significantly different from the control (untreated) ulcer index of 4.3. Therapeutic doses of ranitidine (20 mg/kg) and sucralphate (200 mg/animal) gave an ulcer index of 0.4 and 0.5 respectively. Subtherapeutic doses of ranitidine and sucralphate given in combination yielded an ulcer index of 0.7. Thus, subtherapeutic doses of ranitidine and sucralphate given in combination had a synergistic effect equal to therapeutic doses of each of these drugs given alone. The therapeutic implications of combined acid inhibiting drugs with mucosal protective drugs is discussed.

Aluminum↗
PubMed1990

Diarrhoea of famine and malnutrition: investigations using a rat model. 1. Jejunal hypersecretion induced by starvation.

The effects of progressive starvation for up to three days on the secretory functions of the intestine were investigated using in vitro and in vivo preparations of rat jejunum and secretagogues whose action was either through cyclic AMP or Ca++. Initial starvation for 24 h (day 1) did not significantly alter the basal net electrogenic ion secretion measured in vitro as the short circuit current (Isc, muamps/cm2) or the change in electrogenic ion secretion (delta Isc) induced by the secretagogues. By day 2 of starvation, however, the maximum delta Isc transient induced by the cholinergic and other secretagogues (delta Isc = Isc max-basal Isc) was greatly increased (up to a maximum of 117%) compared with the fed controls on an area basis. The delta Isc were even greater on day 3 of starvation. If a tissue weight basis was used to normalise the data the increase became even more marked. The enhancement in secretion was not caused by a decrease in absorptive capacity as glucose, added mucosally, gave larger increases in absorptive currents in the starved than in the fed jejuna. Bethanecol dose-delta Isc response curves in fed and starved jejuna showed an increase in the maximum electrogenic secretion in the starved but no apparent change in the affinity of their cholinergic receptors mediating the enhanced secretion. The starvation-induced increase in secretion elicited by bethanecol was blocked by atropine, indicating that the receptors were muscarinic, but was unaffected by tetrodotoxin indicating that the enteric neural innervation was not essential for its expression. Noradrenaline released by tyramine was greater in the starved than the fed jejunum, suggesting that a decreased sympathetic tone was unlikely to be the major cause of the starvation induced secretory enhancement. Measurement of jejunal fluid movements in vivo showed that in fed controls and throughout the three days of starvation there was an unchanged net fluid absorption in the basal, unstimulated state. By day 2 and day 3 of starvation, however, bethanecol stimulated fluid secretion was very much greater than that of the fed controls. This increase in fluid secretion was concomitant with significant increases in the concentration of chloride in the lumenal fluid. Starvation thus appears to make the rat jejunum hypersensitive to cholinergic and other secretagogues, increasing the electrogenic secretion of chloride in vitro and that of chloride and fluid in vivo. These results obtained with the rat model give a new insight into possible mechanisms by which the diarrhoea of human famine and malnutrition may be expressed.

Animals↗
PubMed1990

Diarrhoea of famine and malnutrition--investigations using a rat model. 2--Ileal hypersecretion induced by starvation.

The effects of progressive starvation for up to three days on the basal and secretagogue stimulated secretory functions of the rat ileum were investigated in vitro and in vivo. The secretagogues used included agents acting via cyclic AMP (dibutyryl cyclic AMP, theophylline, forskolin, and PGE2) and those acting via Ca++ (acetylcholine, bethanecol, carbachol, 5-hydroxytryptamine, and A23187). Starving rats for 24 h (day 1) had no effect on the basal electrogenic secretion (measured as the short circuit current, Isc muamps/cm2) or on the stimulated maximum electrogenic secretion (measured as the delta Isc where delta Isc = maxIsc-basal Isc). By day 2 of starvation, however, both the basal Isc and the delta Isc induced by all the secretagogues were significantly greater than in the fed and increased even more on day 3. Replacement of all the chloride ions and inhibition by furosemide indicated that the enhanced secretion was due mainly to chloride ions. Cholinergic stimulation was blocked by atropine, indicating the stimulation was via muscarinic receptors while cholinergic dose - delta Isc response curves for fed and starved ilea showed significantly increased maximum electrogenic secretory response in the latter but no evidence of any change in the affinity (ED50) of the receptors mediating the response. The basal secretion and the secretory response to acetylcholine in both fed and starved ilea was unaffected by tetrodotoxin, revealing that the enhanced secretory response could be expressed via the muscarinic receptors on the enterocytes without the enteric neural network. Measurement of ileal fluid movement in vivo showed that in fed and day 1 starved rats the basal, unstimulated 'tone' of the ileum was absorptive. On day 2, however, the basal 'tone' had reversed to one of secretion which increased further on day 3. Stimulation of fluid secretion in vivo by bethanecol, carbachol, or PGE2 induced larger increases in the starved ilea by day 2 which increased even further on day 3. Lumenal chloride and bicarbonate concentrations were greater in the starved ileal fluid than in the fed. The studies in rat ileum confirm and extend those on rat jejunum and indicate that starvation creates a hypersensitive small bowel that responds to secretagogues and cholinergic neurotransmitters with a greatly enhanced secretory response.

Acetylcholine↗
PubMed1991

Vitamin A deficiency and small intestinal secretory function in the rat.

The influence of vitamin A on the functions of the small intestine was examined in rats made vitamin A deficient for 40 days by feeding a special diet after weaning and in pair fed vitamin A deficient rats that were given supplementary vitamin A (240 IU/day) in their drinking water. The basal and stimulated electrogenic secretory and absorptive functions of the jejunum and proximal and distal ileum removed from these rats were examined in vitro using the short circuit current as the index of transport activity. The basal short circuit current in the jejunum and proximal ileum was not significantly different but that of the distal ileum was lower. Electrogenic glucose transfer was not significantly affected by the vitamin deficiency. Cholinergic stimulation using the M1/M2 agonist bethanechol showed a greatly enhanced electrogenic secretion in the jejunum of the deficient rats while secretion stimulated by dibutyryl cyclic adenosine monophosphate was significantly greater in their distal ilea compared with the supplemented group. The vitamin deficiency also disrupted the normal higher/lower hierarchical pattern of transport activity between the proximal and distal ileum. The enhanced secretory activity of the vitamin A deficient small intestine offers a putative explanation for the well known relation between vitamin A deficiency and diarrhoea found in humans.

Animals↗
PubMed1992

Vitamin A deficiency and colonic electrogenic absorption and secretion in the rat.

The effects of vitamin A deficiency on electrogenic transport in the colon were examined in rats made vitamin A deficient at weaning by feeding a vitamin A deficient diet for 40 days. A pair fed control group was given the same diet but supplemented with soluble vitamin A in their drinking water. The basal and stimulated electrogenic secretory and absorptive functions of the muscle stripped proximal, mid, and distal colon were examined in vitro using the short circuit current (Isc) as the index of net ion transport. A significant increase in the basal and secretory Isc (mainly Cl-ions) induced by the cholinergic agonist bethanechol was observed in the mid-colon of the vitamin A deficient rats. In the distal colon, however, vitamin A deficiency caused a significant reduction in both the basal and secretory Isc response to bethanechol compared with the vitamin A supplemented pair fed control. Secretory Isc induced by dibutyryl cyclic adenosine monophosphate was not significantly altered by vitamin A deficiency. The condition abolished the response of the distal colon to luminal amiloride (0.1 mmol/l). Thyroid hormone induced reduction in the distal colonic response to aldosterone is implicated in this lack of response. This is the first experimental linkage between vitamin A action, the thyroid hormone and aldosterone on colonic function. The colonic changes induced by vitamin A deficiency, namely hypersecretion and a reduced electrogenic distal absorptive function, together with the previously described small intestine hypersecretion may be the underlying basis for the diarrhoea observed in human and animal vitamin A deficiency.

Aldosterone↗
PubMed1992

Intestinal hypersecretion of the refed starved rat: a model for alimentary diarrhoea.

Fluid transport was gravimetrically measured in vivo in the duodenum, jejunum, and ileum of anaesthetised fed, 72 hour starved and 72 hour starved rats refed for up to five days after starvation. Basal unstimulated fluid transport was monitored by instilling 0.9% NaCl into the lumen and measuring the gain or loss in weight of the closed intestinal loop. Fluid was absorbed in all the areas of the intestine in the fed rats. Increasing basal fluid absorption was observed in the duodenum over the three days of starvation but in the jejunum there was no significant change. In the ileum, the pattern was very different, on day 1 the fluid was absorbed but on days 2 and 3 there was an increasing secretion of fluid. Refeeding the rats with their normal diet restored the basal absorption of fluid in the duodenum within 24 hours, had no effect in the jejunum but in the case of the ileum the hypersecretion of fluid observed in the day 3 starved rat was maintained on day 1 of refeeding, increased further on day 2, decreased on day 3 but returned to absorption on day 4. The normal absorption was restored to the ileum on day 5 of refeeding. Fluid secretion was induced in all the rat groups by bethanechol (ip 60 micrograms/kg bw) a stable cholinergic agonist, PGE2 (ip 10 micrograms/kg (bw) and E coli STa (luminally instilled, 500 ng/ml) a secretory enterotoxin. All the secretagogues gave enhanced secretion compared with the fed by day 2 of starvation which increased considerably on day 3. Refeeding returned their secretion back to the fed level in the duodenum within 24 hours, in the jejunum within 48 hours but in the ileum their induced secretion on day 2 of refeeding was greater than that of the day 2 of refeeding was greater than that of day 3 starved and took until day 4 to return to the fed levels for behanechol and PGE2 and until day 5 for E. coli STa. This behaviour of rat small intestine showing even greater hypersecretion in the refed state than the starved mimics the human condition of alimentary induced diarrhoea where incautious feeding of starved humans induces severe, often lethal diarrhoea. The refed starved rat appears to be a possible model for this condition.

Animals↗
PubMed1993

Effects of serotonin on rat ileocolonic transit and fluid transfer in vivo: possible mechanisms of action.

The aim was to investigate the action of serotonin (5HT) on function of the ileocolonic junction (ICJ) in vivo. In anaesthetised rats, models were developed to study the effects of intra-aortic (ia) serotonin on ileocolonic and colonic transit, and the effects on transit of a number of 5HT receptor antagonists. In the first series of experiments, a bolus of saline labelled with 99mTc DTPA was instilled 20 cm proximal to the ICJ and transit was assessed three hours later by the geometric centre of the spread of isotope. In the second series, similar techniques were used on the postcaecal colon and transit assessed two hours later. In the third series of experiments, the effects of ia 5HT on ileal net fluid flux was evaluated by standard perfusion experiments with 14C polyethylene glycol (PEG) 4000 as a non-absorbable marker in rat plasma-like electrolyte solution. Compared with ia saline, 5HT accelerated ICJ transit significantly (p < 0.05). This acceleration was comparable with the effect of ia bethanechol. The effects of 5HT on ICJ transit were inhibited by the intraperitoneal (ip) infusion of atropine, the 5HT receptor antagonists, methysergide, ketanserin, zacopride, and the 5HT4 agonist, SC53116. Methysergide, zacopride, and SC53116 given with ia 5HT slowed ICJ transit to rates below those of ia saline alone. When these same agents were given together with ia saline, the ICJ transit was not significantly altered. Serotonin, at the dose that accelerated ICJ transit, did not significantly alter colonic transit or ileal fluid transport. In conclusion, 5HT is a potent pharmacological stimulant of transit across the rat ICJ in vivo; the action of 5HT is mediated partly through muscarinic neurones and several 5HT receptor subtypes.

Animals↗
PubMed1993

Regulation of gall bladder motility by the arginine-nitric oxide pathway in guinea pigs.

Nitric oxide (NO) synthesised from L-arginine is an intercellular messenger in various biological actions including endothelial dependent relaxation and inhibition of platelet aggregation. This study explored the role of the L-arginine-NO pathway in the regulation of gall bladder motility. Intraluminal gall bladder pressure was recorded in anaesthetised guinea pigs in response to cholecystokinin or bethanechol before and after treatment with specific NO synthase inhibitors (NG-nitro-L-arginine, NG-nitro-L-arginine methyl ester, or NG-monomethyl-L-arginine), or with an NO donor (sodium nitroprusside). Baseline gall bladder pressure significantly increased after treatment with the NO synthase inhibitors. Responses to cholecystokinin (0.025-1.25 nmol/kg) were significantly enhanced after treatment with NG-nitro-L-arginine methyl ester and lasted two to threefold longer than in control experiments. The effect of the inhibitor both on resting pressure and on cholecystokinin induced changes was reversed by L-arginine but not by D-arginine. Pretreatment with the inhibitors also induced a significant enhancement of the response to bethanechol. On the other hand, sodium nitroprusside abolished the response to low dose cholecystokinin and reduced the response to a high dose by about 80%. In vitro experiments with isolated gall bladder strips showed a significant enhancement of the contractile response to cholecystokinin or bethanechol after preincubation with the NO synthase inhibitor. Calcium dependent activity of NO synthase was detected in fresh homogenates from gall bladder tissue and incubation with endotoxin induced considerable calcium independent activity. These findings support the existence of a key L-arginine-nitric oxide pathway regulating gall bladder contraction.

Amino Acid Oxidoreductases↗
PubMed1978

Evidence for a change in neurotransmitter affecting oesophageal motility in Parkinson's disease.

In a study of oesophageal motility in 20 patients with Parkinson's disease, intravenous atropine produced marked disruption of co-ordination in response to swallows, when compared with control subjects. This suggests that cholinergic rather than dopaminergic mechanisms are more important in the control of swallowing in patients with Parkinsonism. No conclusive evidence of peripheral dopamine depletion or autonomic neuropathy was found, although minor changes suggestive of the former were found in severely affected patients.

Aged↗
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↗
PubMed1984

Secretagogues cause a preferential discharge of large size granules in rat pancreas.

We have compared the diameters of zymogen granules in the exocrine pancreas of fasted or stimulated rats. The average granule diameter was 0.73 microns +/- 0.18 SD (sample size, 1460) in fasted animals and significantly reduced to 0.68 microns +/- 0.17 SD (sample size, 860) after 120 min and two intraperitoneal injections of urecholine. Reduction of granule size was attributable to the preferential discharge of large size granules. The range between first and third quartiles of the distribution curve was identical in the two groups at 0.24 microns. There was no significant increase in the proportion of granules smaller than 0.40 microns after urecholine stimulation. A third group of animals was "hyperstimulated" by an infusion of a mixture of caerulein, secretin, and urecholine. After 210 min, the average granule diameter was reduced to 0.43 microns +/- 0.14 SD (sample size, 786). The range between first and third quartiles of the distribution curve was 0.16 microns. In this group, 43.5% of the granules was smaller than 0.40 microns. Granule size reduction was accompanied by the appearance of numerous pleiomorphic condensing vacuoles. The present results strongly support the views that secretagogues cause the preferential release of large size granules and favor the formation of small size granules.

Animals↗