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 109 records · Page 6Linked to original sources
PubMed1989

Central and peripheral muscarinic actions of physostigmine and oxotremorine on avoidance responding of squirrel monkeys.

The involvement of central and peripheral muscarinic cholinergic receptors in the behavioral effects of the cholinesterase inhibitor physostigmine was evaluated by comparing the ability of atropine and methylatropine to reverse the effects of physostigmine, the muscarinic agonist oxotremorine, or their quaternary analogs neostigmine and oxotremorine-M. Avoidance behavior was maintained under a schedule in which every lever press postponed delivery of electric shock for 20 s; shock occurred every 5 s in the absence of responding. Cumulative doses of physostigmine or oxotremorine produced dose-related decreases in response rates, and increases in response durations and rates of shock delivery. Similar effects occurred with neostigmine and oxotremorine-M. Methylatropine completely prevented the behavioral and parasympathetic effects of neostigmine and oxotremorine-M without having any behavioral effects of its own. However, methylatropine did not alter the behavioral effects of physostigmine or oxotremorine. Atropine prevented the peripheral manifestations as well as the behavioral effects of physostigmine and oxotremorine even though atropine decreased avoidance responding when given alone. These results suggest that in squirrel monkeys, central and peripheral muscarinic receptors may function in a redundant manner to control agonist-induced decrements in avoidance. When physostigmine or oxotremorine was given in conjunction with atropine, rates of avoidance responding were increased to 180% of control levels. Response rate increases after administration of oxotremorine or physostigmine in monkeys treated with atropine may reflect a non-muscarinic action of atropine, unmasked by the presence of cholinomimetics.

Animals↗
PubMed1976

Mechanisms of tyrosine hydroxylase and dopamine beta-hydroxylase induction in organ cultures of rat sympathetic ganglia by potassium depolarization and cholinomimetics.

It was the aim of the present study to elucidate the mechanisms involved in specific tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) induction by potassium depolarization and cholinomimetics in rat superior cervical ganglia kept in organ culture. The effect of high (54 mM) potassium concentration on intact ganglia seems to result in a dual action: a) a specific induction of TH and DBH via release of acetylcholine from preganglionic cholinergic nerve terminals. b) a non-specific effect on terminal adrenergic neurons resulting in a general increase of protein synthesis as indicated by the increase in DOPA decarboxylase (DDC) and monoamine oxidase (MAO) activities. In decentralized superior cervical ganglia potassium depolarization failed to produce the specific TH and DBH induction although a small increase in DDC activity persisted. Carbamylcholine, acetylcholine and nicotine at concentrations of 10(-4) M elicited a selective induction of TH and DBH both in intact and decentralized ganglia via nicotinic receptor stimulation. Bethanechol, predominantly stimulating muscarinic receptors had no significant effect on TH activity. A 4 h pulse of 10(-4) M carbamylcholine produced optimal induction of DBH and TH 24 h and 48 h later respectively. Longer exposure to carbamylcholine resulted in a significantly smaller rise in TH activity.

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↗
PubMed1984

Evidence for two opposite effects of clonidine on gastric acid secretion in the dog.

The effects of clonidine on gastric acid secretion were studied in conscious dogs with both gastric fistulae and Heidenhain pouches. Clonidine infused systemically at graded doses under basal conditions produced a significant increase in acid secretion from both gastric fistulae and Heidenhain pouches. Acid secretion from gastric fistulae submaximally stimulated by pentagastrin was dose-dependently reduced by clonidine while 2-deoxy-D-glucose-induced secretion was completely suppressed. Under these conditions a significant enhancement of secretion from Heidenhain pouches was recorded. An increase in acid secretion from both main stomachs and Heidenhain pouches was observed for clonidine with submaximal doses of bethanechol and histamine as stimulants, though clonidine showed no effect on maximal stimulation by histamine. The stimulant effect of clonidine from gastric fistulae and Heidenhain pouches under basal conditions was fully prevented by cimetidine, while the inhibitory effect of clonidine on acid secretion stimulated by pentagastrin from gastric fistulae was reversed by yohimbine. The present results suggest that clonidine displays two simultaneous yet opposite effects on dog gastric secretion. The inhibitory effect might be mediated through a decrease of vagally released acetylcholine following the activation of alpha 2-adrenoceptors both at central and peripheral sites, while the stimulatory effect probably depends on the histamine-like properties of the drug.

Animals↗
PubMed1978

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

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

Action Potentials↗
PubMed1984

Role of muscarinic cholinergic mechanisms in the substantia nigra pars reticulata in mediating muscular rigidity in rats.

Bethanechol chloride (5-25 micrograms), when injected into the substantia nigra pars reticulata (SNR) of rats, produced muscular rigidity in a dose-dependent way, and in addition, catalepsy and ipsilateral posture. The effects of bethanechol in the dose of 25 micrograms were prevented by co-administration of 10 micrograms scopolamine hydrochloride. Injections of 25 micrograms bethanechol or 10 micrograms scopolamine into the reticulata only slightly affected the muscular rigidity produced by 15 mg/kg i.p. morphine hydrochloride. The results suggest that muscarinic cholinergic mechanisms in the substantia nigra pars reticulata, although effective by themselves, affect by expression of at least one striatal functional alteration, the muscular rigidity, in a less effective way than GABAergic or endogenous opioid mechanisms do.

Animals↗
PubMed1981

The extraneuronal O-methylation of 3H-(+)isoprenaline by guinea-pig tracheal rings in vitro.

Tracheal rings isolated from male guinea-pigs and incubated in Krebs' solution at 37 degrees C O-methylated 3H-(+/-)-isoprenaline by a saturable, high affinity mechanism. 1. With 3H-isoprenaline at 1 mumol . 1-1, O-methyl 3H-(+/-)isoprenaline (3H-OMI) appeared in the tissue with a half-time for approach to steady state of approximately 10 min and was measured in the incubation medium after about 5 min, its concentration increasing linearly thereafter. With 3H-isoprenaline concentrations ranging from 1 to 200 mumol . 1-1, the total formation of 3H-OMI (estimated from that contained in the tissue and the medium) was maintained at steady state rates for up to 60 min, after initial lag times of between 1 and 3 min. O-methylation obeyed Michaelis-Menten saturation kinetics; Km = 6.14 +/- 0.13 mumol . 1-1, Vmax = 0.31 +/- 0.01 nmol . g-1 . min-1. 2. The catechol-O-methyl transferase (COMT) inhibitor U-O521 and the extraneuronal uptake inhibitor corticosterone both reduced O-methylation of 3H-isoprenaline (0.1 mumol . 1-1) by tracheal rings. However, U-O521 was fully inhibitory (IC50 = 2.6 mumol . 1-1), but corticosterone inhibited by only 46% at concentrations up to 1 mmol . 1-1. 3. The O-methylating activity of the "smooth muscle-rich" component of the trachea was approximately three-times greater than for complete tracheal rings. However, considerable activity was also associated with "cartilage-rich", "smooth muscle-poor" sections. This activity did not seem to be associated with endothelial cells. 4. Histamine strongly inhibited O-methylation (IC50 = 30 mumol . 1-1), but two other contractile agonists, 5-hydroxytryptamine and bethanechol, were weakly active and inactive, respectively.

Animals↗
PubMed1979

Exogenous and endogenous stimulations during different phases of pancreatic secretion in conscious rats.

The effects of stepwise increasing doses of intravenous caerulein, secretin, urecholine and intraduodenal oleic acid were investigated in conscious rats. a) Basal water, bicarbonate, and protein secretion significantly augmented after diversion of pancreatic juice. On the basis of protein secretory pattern of basal secretion 3 stable stages have been recognised: 1. The most physiological basal stage during return of pancreatic juice. 2. The first, highly elevated plateau from the 4th to 7th 30-min period after diversion of pancreatic juice. 3. The second, delayed and less elevated plateau after 270 min. b) The following patterns of stimulated secretion were observed: 1. Caerulein stimulated protein and bicarbonate secretion during return of juice and the first plateau but it failed to elicit a significant response during the second, delayed plateau. 2. Secretin and urecholine showed similar protein responses during return of pancreatic juice but after diversion, they stimulated water and bicarbonate secretion only. 3. During the second plateau oleic acid stimulation resulted in a significant increase in water and bicarbonate secretion but no significant increase occured in protein output. The delayed inhibition of protein secretion, previously described in our laboratory, was unchanged. 4. Supramaximal doses of exogenous stimuli caused an inhibition in pancreatic secretion.

Animals↗
PubMed1985

Cholinergic control of gastric acid secretion.

In the perfused stomach preparation of the anaesthetized rat the cholinergic agonists acetylcholine (ACh) and bethanechol stimulated gastric acid secretion. Both agonists produced similar maximal acid output (70 mumols/15 min) when infused intravenously. However, bethanechol was more potent, eliciting half maximal stimulation at 1.98 mumols/kg/h, while the corresponding dose of ACh was 10.95 mumols/kg/h. Secretory responses to either agonist were antagonized in a dose related fashion by blockade of muscarinic receptors with atropine. In contrast, inhibition of nicotinic receptors with hexamethonium produced a striking potentiation of ACh stimulated secretion whilst the bethanechol elicited secretion remained unaffected. In the presence of full nicotinic receptor blockade the ACh response curve was shifted to the left sixfold, half maximal stimulation being produced at 1.79 mumols/kg/h. Cimetidine partially inhibited the secretory responses elicited by either ACh or bethanechol while blockade of adrenoceptors (alpha and beta) did not affect acid output induced by cholinergic agonists. Secretion elicited by ACh is interpreted as being the composite effect of pro-secretory action and an inhibitory mechanism due to the activation of nicotinic receptors. Hexamethonium, through nicotinic receptor blockade, inhibits the restricting mechanism and thus reveals the full stimulatory action of ACh.

Acetylcholine↗
PubMed1982

Hidradenitis suppurativa: evidence for a bactericidal defect correctable by cholinergic agonist in vitro and in vivo.

Hidradenitis suppurativa (HS) affects the apocrine sweat glands, giving chronic recurrent abscesses of axillary and perineal areas. We report a patient who had a defect in polymorphonuclear leukocyte killing of bacteria associated with low levels of intracellular cyclic GMP. This defect was corrected with a cholinergic agonist in vitro. Treatment of the patient with a cholinergic agonist, bethanechol chloride, resulted in prolonged clinical improvement, normal bactericidal function, and normal levels of intracellular cyclic GMP. The possible mechanisms responsible for the bactericidal defect and for the patient's improvement are discussed.

Aged↗
PubMed1975

Cholinergic stimulation of the lower esophageal sphincter in patients with vagotomy and antrectomy.

Recently cholinergic stimulation of the lower esophageal sphincter (LES) with bethanechol has been shown to be effective in the treatment of chronic gastroesophageal reflux. Since chronic reflux and esophagitis also occur in patients with vagotomy and antrectomy, we studied the effect of bethanechol on sphincter pressure in 10 patients who had had vagotomy and antrectomy. Both subcutaneous (0.08 mg/kg) and oral (25 mg) administration of bethanechol caused significant increases in LES pressure in these patients. In addition, both subcutaneous and oral administration of bethanechol elevated hypotensive sphincter pressures to normal levels. Orally administered bethanechol produced a sustained increase in LES pressure throughout a 90-min study period. These studies suggest that cholinergic stimulation of the LES with bethanechol may be of therapeutic benefit in vagotomized and antrectomized patients with gastroesophageal reflux.

Administration, Oral↗