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 883 records · Page 49Linked to original sources
PubMed1988

Synergism between calcium-mediated and cyclic AMP-mediated activation of chloride secretion in isolated guinea pig distal colon.

Synergistic effects of Ca2+-mediated secretagogues and cyclic AMP-mediated secretagogues on Cl- secretion by guinea pig distal colon were studied in vitro using Ussing chambers. Short-circuit current (Isc) and bidirectional fluxes of 22Na+ and 36Cl- were measured. Bethanechol (10(-4) M, a Ca2+-mediated secretagogue) caused an increase in Isc, which was enhanced 4-20 fold when the tissue was pretreated with prostaglandin E2 (10(-7)-10(-6) M), vasoactive intestinal polypeptide (5 x 10(-9)-10(-8) M) (cyclic AMP-mediated secretagogues), or 8-bromocyclic AMP (5 x 10(-4)-2 x 10(-3) M). Measurement of 36Cl flux showed that the increase in Isc in the presence of both 8-bromocyclic AMP and bethanechol resulted principally from increased Cl- secretion. On the other hand, the net absorptive flux of 22Na was not influenced under these conditions. Potentiation of the increase in Isc was also elicited by the combination of A23187 (5 x 10(-6) M) and 8-bromocyclic AMP (10(-3) M). The results are consistent with the notion that simultaneous activation of the cyclic AMP-mediated and Ca2+-mediated systems produces a synergistic increase in colonic Cl- secretion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Muscarinic stimulation and antagonism and glucoregulation in nondiabetic and obese hyperglycemic mice.

Plasma glucose and insulin responses to a muscarinic agonist (bethanechol chloride) and a muscarinic antagonist (atropine) were evaluated in obese C57BL/6J ob/ob mice and in lean C57BL/6J + /? mice. In lean +/? mice, plasma glucose decreased in response to 1 and 2 micrograms/g bethanechol chloride, whereas insulin increased significantly. In ob/ob mice, insulin increased remarkably in response to bethanechol administration (saline, 632 +/- 80 microU/ml; 2 micrograms/g bethanechol chloride, 1794 +/- 97 microU/ml; n = 10), but surprisingly, plasma glucose also rose significantly (saline, 230 +/- 14 mg/dl; 2 micrograms/g bethanechol chloride, 363 +/- 18 mg/dl, n = 10). This exaggerated hyperglycemia in ob/ob mice was not associated with significant changes in plasma glucagon. Furthermore, administration of propranolol hydrochloride did not diminish bethanechol chloride-induced hyperglycemia in ob/ob mice. Administration of atropine (2.5, 5, and 10 mg/kg body wt) induced a significant decrease in plasma insulin without changes in plasma glucose in ob/ob mice, whereas neither plasma insulin nor plasma glucose changed in lean mice. Finally, conversion of [14C]alanine to glucose was increased in ob/ob mice after bethanechol chloride administration, indicating that muscarinic stimulation increases gluconeogenesis in an animal model of type II (non-insulin-dependent) diabetes.

Animals↗
PubMed1989

Insulin prevention of altered muscarinic receptor-G protein coupling in diabetic rat atria.

Right atria from rats rendered diabetic by injection of streptozocin (STZ-D) for 8-10 wk are supersensitive to the negative chronotropic effects of muscarinic agonists but have decreased levels of muscarinic receptors and acetylcholinesterase activity. Insulin treatment completely prevents the development of these changes. The proportion of atrial muscarinic receptors displaying high-affinity agonist binding is lower in STZ-D rats; however, the sensitivity of high-affinity agonist binding to regulation by a guanine nucleotide (5'-guanylylimidodiphosphate) is greater in atria from diabetic rats. Again, insulin treatment eliminates these differences. These findings indicate that alterations in atrial muscarinic systems in STZ-D rats are a consequence of the elaboration of the diabetic state and suggest that an alteration of functional muscarinic receptor-G protein coupling contributes to the altered physiological responsiveness of the heart in diabetes.

Acetylcholine↗
PubMed1989

Effects of diabetes and diuresis on contraction and relaxation mechanisms in rat urinary bladder.

Experiments were designed to gain information on the mechanisms leading to diabetic urinary bladder dysfunction. Bladders from control rats, animals subjected to 4-5 wk streptozocin-induced diabetes, and rats subjected to equivalent diuresis produced by 5% sucrose feeding were studied with an in vitro whole-bladder preparation and neurochemical measurements. The diuretic group was used to distinguish alterations produced by metabolic effects on nerve and muscle from those induced by prolonged periods of excessive diuresis. Diuresis alone explains many of the diabetes-induced effects, including decreased norepinephrine levels, postsynaptic supersensitivity for sympathetic regulation of bladder storage, decreased responsiveness to parasympathetic regulation of emptying, and enhanced prostaglandin F2 alpha-induced contraction. Other diabetes-induced effects were not observed in the diuretic controls and are presumed to result from metabolic alterations associated with diabetes. These effects were decreases in norepinephrine uptake and in choline acetyltransferase activity, both markers of nerve terminal function. Thus, diuretic and metabolic factors appear to contribute to the early signs of parasympathetic and sympathetic neuropathy. In contrast, we found no evidence for loss of sensory nerve function in the diabetic bladder, at least at the organ level, because no diabetes- or diuresis-induced changes were observed in responsiveness to substance P or capsaicin.

Aminophylline↗
PubMed1990

Adaptation of cholinergic enteric neuromuscular transmission in diabetic rat small intestine.

Representative longitudinal muscle strips (6 x 10 mm) from distal small intestine were obtained from rats after 1, 2, and 3 mo of streptozocin-induced diabetes. The strips were stretched to their optimum lengths and subjected to electrical field stimulation (1-ms pulse duration, 30-270 mA, 10 Hz) in the presence of Krebs solution and Krebs solution plus 10(-6) M atropine. Field stimulation produced atropine-sensitive and atropine-resistant contractions in all strips. After 1 mo, significant differences in the amplitudes of the atropine-sensitive contractions were found between the diabetic rats and nondiabetic controls. Insulin-treated diabetic rats showed contraction responses that were intermediate in amplitude. After 2 mo, the difference between the control and diabetic groups was less evident but still significant. After 3 mo, the previously noted difference in the atropine-sensitive contractions between the diabetic and control groups had resolved. No significant differences among the three groups were noted in the amplitudes of the atropine-resistant contractions. Field stimulation delivered at pulse durations of 50 ms in the presence of neural blockade with tetrodotoxin (5 x 10(-6) M) produced similar contraction amplitudes among the three groups at any respective time phase of the study. Dose-response studies of intestinal muscle after 3 mo of untreated diabetes showed normal tension development to both bethanechol chloride and physostigmine. These results indicate that streptozocin-induced diabetes is acutely associated with defective cholinergic neuromuscular transmission in the myenteric plexus of the distal small intestine. The abnormality is less evident after 2 mo of untreated diabetes and resolves spontaneously after 3 mo. Insulin treatment appears to accelerate this resolution.

Animals↗
PubMed1978

The measurement of resting and stimulated lower esophageal sphincter pressure using the rapid pull-through technique of esophageal manometry.

The value of the rapid pull-through technique of esophageal manometry for the measurement of lower esophageal sphincter pressure (LESP), in the diagnosis of symptomatic gastroesophageal reflux, has been investigated. The technique provides reproducible measurements of LESP in individual subjects during the period of a single recording study. It does not discriminate between normal subjects and patients with symptomatic gastroesophageal reflux in measurements of basal LESP or in measurements of the LESP response to abdominal compression and the cholinergic drugs bethanechol and metoclopramide. The findings of the study suggest that the rapid pull-through technique will not prove helpful in the diagnosis of symptomatic reflux.

Adult↗
PubMed1980

'Non-active' pepsin secretion compared with stimulated secretion by bethanechol, histamine, pentagastrin, and 2-deoxy-D-glucose. The role of vagal innervation.

The present studies were performed on a double-pouch dog with one vagally innervated Amdrup pouch (AP) and one denervated Heidenhain pouch (HP), allowing comparison of pepsin secretion from innervated and denervated mucosa at the same time in the same animal. 'Non-active' secretion of pepsin was determined by instillation in the pouches of 0.1 M and 0.005 M HCl, 0.15 M NaCl, and 0.03 M phosphate buffer, and well-known stimulators of gastric secretion such as histamine, pentagastrin, bethanechol, and 2-deoxy-D-glucose (2-DG) were tested as pepsigogues. Cholinergic stimulation by 2-DG and bethanechol (Urecholine) was clearly the most potent stimulus of pepsin secretion. 2-DG elicited secretion only from innervated mucosa, whereas the responses to bethanechol were similar in the two pouches. Histamine and pentagastrin were weak stimulators, but both provoked active and sustained secretion of pepsin when given in small doses. Higher doses of histamine strongly inhibited pepsin output. The effects of histamine were independent of vagal innervation. By contrast, the active stimulation by pentagastrin only took place in innervated mucosa. The highest outputs were seen in the lowest doses, but also very high doses of pentagastrin elicited active pepsin secretion in the AP. Medium doses of pentagastrin brought the secretion down the the 'non-active' level. The chief cells in the denervated mucosa were quite insensible to pentagastrin, and the pepsin output in the HP equalled the non-active' response at all dose levels.

Animals↗
PubMed1981

Effect of a beta2-sympathomimetic on urecholine-stimulated gastric acid secretion in dogs.

The effect of a selective beta2-adrenoceptor agonist on urecholine-stimulated gastric acid secretion was studied in conscious gastric fistula dogs. A dose-dependent inhibition was found, most pronounced for the highest doses of urecholine. The inhibition was primarily on volume, whereas the acidity showed a decreasing tendency only. The pulse rate was increased by the beta2-agonist and by urecholine in high doses. Propranolol prevented both the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with five doses of urecholine and two doses of the beta2-agonist showed a decrease in maximal response, and transformation of the curve suggested an unchanged D50. It is concluded that the beta2-agonist inhibits urecholine-stimulated acid secretion in the dog to the same degree as pentagastrin-induced acid secretion, and much stronger than found for histamine-induced acid secretion in earlier experiments. The inhibition seems to follow a noncompetitive kinetic, and beta2-receptors are probable involved.

Adrenergic beta-Agonists↗
PubMed1981

Cholinergic secretory and inhibitory mechanisms in canine pancreatic secretion.

Dose-response relationships for pancreatic stimulants and the interactions by atropine were studied in conscious gastric and duodenal fistula dogs. Secretin, caerulein, and bethanechol, the two latter against background secretin, induced similar maximal secretions of water and bicarbonate, and maximal protein outputs with the two latter were not different. Actions of atropine differed according to type and dose of stimulant, dose of atropine, and secretory variable studied. In the dose interval of 10-40 microg x kg(-1) x h(-1), atropine suppressed the secretin-stimulated water and bicarbonate, but these or lower doses enhanced the response to submaximal caerulein. The secretion after 200 microg x kg(-1) x h(-1) or less bethanechol was unaffected by atropine, but the suppressed response to higher bethanechol doses was reversed and enhanced. These findings are compatible with the presence of one ductal secretory process sensitive to cholinergic influence in three ways: one secretory, partly atropine-sensitive, required for submaximal secretin's optimal action; one secretory, stimulated by bethanechol, and atropine-resistant; and one inhibitory, atropine-sensitive, triggered by caerulein (and high doses of bethanechol). Atropine at low doses inhibited the protein output by bethanechol but enhanced the submaximal caerulein response, which again indicates the presence of an inhibitory atropine-sensitive cholinergic principle. It is proposed that pancreatic polypeptide may be the mediator of this inhibition and that vasoactive intestinal polypeptide could be the mediator of the atropine-resistant cholinergic stimulation of water and bicarbonate secretion.

Animals↗
PubMed1982

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

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

Adrenergic beta-Antagonists↗
PubMed1982

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

The aim of the present study was to investigate the effect of Dopamine on bethanechol-stimulated gastric acid secretion and mucosal blood flow. dopamine was used alone and in conjunction with selective blockade of the alpha, beta, and dopaminergic receptors. An increasing and dose-dependent stimulation of gastric acid secretion was found for dopamine at 1, 5, and 10 micrograms/kg/min. A significant inhibition of gastric acid secretion was found with the highest dose of dopamine (40 micrograms/kg/min). the stimulatory effect seems to be mediated by more than one receptor, whereas the inhibition by high dopamine doses could be explained by a beta 1 stimulation. Dopamine (10 micrograms/kg/min) was found to increase the bethanechol-stimulated gastric mucosal blood flow. Phentolamine (alpha blackade) increased this dopamine-elevated blood flow further, with a significant increase in the ratio between blood flow and acid secretion, indicating a primary action of the alpha receptors on blood flow. Bethanechol stimulated the gastric acid secretion and blood flow in a parallel manner. It is concluded that alpha-receptor stimulation is the predominant directly acting factor in the regulation of gastric mucosal blood flow, whereas stimulation of beta, muscarinic, and 'gastrinergic' receptors mainly occurs indirectly via changes in parietal cell function. The main effect of dopamine seems to be on gastric motility, whereas the effect on gastric acid secretion is of minor importance.

Animals↗
PubMed1982

Disappearance of an inhibitory factor of exocrine pancreas secretion in chronic alcoholic dogs.

In non-alcoholic dogs the exocrine pancreatic response to caerulein, but not to urecholine or secretin alone, was increased by atropine. This indicated a pancreatic inhibition triggered by the caerulein stimulation and blocked by atropine. The present aim was to examine whether atropine had a similar action on the caerulein-stimulated pancreatic secretion in dogs submitted to long-term alcohol feeding. Alcohol-fed dogs showed an increased volume and bicarbonate response to submaximal caerulein but a non-modified protein response as compared with the responses before alcohol adaptation. The elevated water and bicarbonate responses were not further enhanced by atropine, which, in contrast, enhanced the responses of normal dogs to such an extent as to equalize their responses with those of the treated dogs. Atropine, 5 micrograms X kg-1 X h-1, enhanced similar protein responses to submaximal caerulein more in normal than in alcohol-fed dogs, but with an eightfold higher atropine dose no enhance was produced in dogs alcohol-fed for 36 months. This dose of atropine still evoked a small and similar enhancement in the normal and 9-month-treated dogs. The enhancing action of atropine on caerulein-stimulated secretion, present in normal dogs, hence diminishes and finally disappears as a result of chronic alcohol feeding.

Alcoholism↗
PubMed1982

Effect of isoprenaline on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of isoprenaline on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility for both frequency and strength. Isoprenaline, a beta 1- and beta 2-agonist, was used alone and in conjunction with selective blockade of beta 1 and beta 2 receptors. The stimulated antral motility was dose-dependently inhibited by isoprenaline. The effect was significantly blocked by the beta 1 + beta 2-adrenoceptor blocker propranolol and by using in conjunction the beta 1-adrenoceptor blocker practolol and the beta 2-adrenoceptor blocker H 35/25. H 35/25 and particularly practolol reduced the effect of isoprenaline to some extent, but the reduction was not of statistical significance. This indicates that isoprenaline acts on antral motility through both beta 2 and beta 1 receptors. Dose-response experiments with five logarithmically increasing doses of bethanechol and one dose of isoprenaline showed inhibition of a non-competitive type.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of dopamine on bethanechol-stimulated gastric antral motility in dogs with gastric fistula.

The purpose of the present study was to evaluate the effect of dopamine on gastric antral motility in conscious dogs with gastric fistula, using intraluminal strain-gauge transducers. Infusion of bethanechol increased the motility with regard to both frequency and strength. Dopamine, an endogenous catecholamine, was used alone and in conjunction with selective blockade of adrenergic and dopaminergic receptors. The stimulated antral motility was dose-dependently inhibited by dopamine. The effect was significantly blocked by the peripherally acting dopaminergic blocker domperidone. The alpha-adrenoceptor blocker phentolamine reduced the effect of dopamine to some extent, but the reduction was not of statistical significance. The dopamine-inhibited motility was not altered by the beta 1-adrenoceptor blocker practolol or the beta 1 + beta 2-adrenoceptor blocker propranolol. This indicates that dopamine acts on gastric antral motility predominantly through dopaminergic receptors. beta-Adrenergic receptors, which are active in the impairment of gastric acid secretion, do not seem to be involved in the motility response. Dose-response investigations with five increasing doses of bethanechol and one dose of dopamine showed inhibition of a non-competitive type.

Adrenergic alpha-Antagonists↗