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At least 307 records · Page 17Linked to original sources
PubMed1985

Effect of the parasympathetic system on secretion of parathyroid hormone.

This study evaluated the effect of parasympathetic agonists and antagonists on immunoreactive (i) PTH secretion in vitro and on serum iPTH in vivo in rats. In in vitro studies pilocarpine or bethanechol significantly inhibited PTH secretion. This inhibition was blocked by the simultaneous addition of atropine to the incubation medium. In in vivo studies, the cholinergic agonists pilocarpine and bethanechol and the cholinergic antagonist atropine were administered to rats by IV infusion. Blood was obtained before and again after two hours of infusion for analysis of iPTH. Pilocarpine or bethanechol significantly decreased serum iPTH. This inhibition by either agent was blocked by the simultaneous administration of atropine. Administration of atropine alone significantly increased serum iPTH above baseline. This stimulation of basal serum iPTH by parasympathetic blockade suggests that even basal PTH secretion may be influenced by endogenous parasympathetic tone. Therefore, the following conclusions were reached: (1) parasympathetic influences inhibit PTH secretion, and (2) endogenous parasympathetic tone may be an inhibitory modulator of basal secretion of PTH.

Animals↗
PubMed1993

The influence of diabetes mellitus on glucose utilization by the rat urinary bladder.

Streptozocin-induced diabetes in rats causes changes in urinary bladder function and increases the responsiveness of isolated bladder strip preparations to contractile agents and field stimulation. We monitored the role of extracellular glucose in the contractile responsiveness of bladder body strips from control, 2-month diabetic, and sucrose-drinking rats to the muscarinic agonist bethanechol. Consumption of sucrose and induction of diabetes caused increases in bladder mass compared with that of controls. In the presence of normal glucose levels (5.6 mmol/L), bladder strips from diabetic rats responded to bethanechol with significantly larger responses than those from control or sucrose-drinking rats. Removal of glucose from the bathing medium caused time-dependent decreases in contractile response of bladder strips from all groups; there were no differences in the percent decrease in response between the three groups. The presence of insulin (100 mU/mL) had no effects on contractile responsiveness or the rate of decline of response. Following return of glucose to the medium, there were progressive increases in contractile responsiveness in all groups, which returned to original contractile values within 60 minutes and were unaffected by insulin. Pyruvate (9.1 mmol/L) was able to substitute for glucose in maintaining the contractile responses. Increasing the glucose concentration of the medium to 30 mmol/L had no effects on contractile responses. Unstimulated bladder adenosine triphosphate (ATP) and creatine phosphate concentrations were similar in control, diabetic, and sucrose-drinking rats. In conclusion, changes in glucose utilization and high-energy phosphate levels cannot explain the increased contractile responsiveness of bladder body strips from diabetic rats to contractile agents.

Adenosine Triphosphate↗
PubMed1986

Gastric acid secretory responses to cholinergic and histaminergic stimulation in chronic morphine-treated rats.

The effects of chronic morphine administration on cholinergic and histaminergic activities were evaluated in rats by observing their gastric acid secretory responses to secretagogues. The responses of in-vivo perfused stomachs to 2-deoxy-D-glucose or pentagastrin, and of the isolated gastric mucosa to histamine or bethanechol, were not significantly different between naive and chronic morphine-treated animals. It is suggested that the chronic morphine-treated rats exhibit normal cholinergic and histaminergic activities as well as receptor sensitivities to acetylcholine and histamine.

Animals↗
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↗
PubMed1993

Pilocarpine and other cholinergic drugs in the management of salivary gland dysfunction.

Sialagogues constitute an important component in the management of salivary gland dysfunction. Of the pharmacologic agents available, pilocarpine has been used extensively over the last century. Many clinical trials have documented the efficacy of this alkaloid, with doses that range from 1 to 15 mg normally taken four times a day. There is considerable individual variation in response although it is usually possible, in the presence of sufficient responsive exocrine tissue, to establish a therapeutic regimen that promotes increased salivation without significant side effects.

Anethole Trithione↗
PubMed1994

A clinical trial of bethanechol in patients with xerostomia after radiation therapy. A pilot study.

The effects of bethanechol in the treatment of dry mouth were assessed in patients with xerostomia after radiation therapy to the head and neck. Bethanechol possesses muscarinic and nicotinic-cholinergic activity that likely accounts for its mode of action. Bethanechol (25 mg, three times daily) was not associated with significant side effects. Statistically significant increases in whole resting saliva (p = 0.003) and whole stimulated saliva (p = 0.001) were seen. In patients with pretreatment stimulated saliva volumes greater than resting saliva volumes, a positive response to subsequent use of the sialagogue was seen.

Bethanechol↗
PubMed1985

The influence of morphine on acid secretion by the isolated rat gastric mucosa.

The influence of morphine on acid secretion by the isolated gastric mucosa was studied in adult rats. A wide range of morphine concentrations (1 X 10(-4) to 1.6 X 10(-3) M) was found to have no effect on basal acid output, or on acid secretion maximally stimulated by bethanechol or histamine. It is suggested that the opiate receptors in the rat gastric mucosa, if there are any, are not involved in modulating acid secretion.

Animals↗
PubMed1992

Loss of absorptive capacity for sodium and chloride in the colon causes diarrhoea in Potomac horse fever.

Ehrlichia risticii, an obligate intracellular bacterium in the family Rickettsiaceae, causes Potomac horse fever which is often associated with severe watery diarrhoea. The mechanism of the diarrhoea is unknown. The aim of this study was to determine whether sodium and chloride transport, morphology and cyclic adenosine 3', 5'-monophosphate (cyclic AMP) content of colonic mucosa was altered in E risticii-infected horses. Mucosa-submucosa sheets from the large and small colon of nine infected and seven to nine uninfected horses were set up in Ussing chambers for measurement of short-circuit current and transepithelial 22Na and 36Cl fluxes. Uninfected tissues absorbed both sodium and chloride whereas absorption of sodium and chloride was abolished in infected tissues. Bethanechol and histamine evoked a concentration-dependent increase in short-circuit current in both groups, but the responses were attenuated at all concentrations in infected horses. Slight focal degeneration of colonic epithelial cells and loss of microvilli from glandular epithelial cells occurred in infected horses. There was a significant increase in cyclic AMP content in colonic mucosa of infected animals. The results suggest that E risticii infection induces focal microscopic degeneration of epithelial cells and an increase in intracellular cyclic AMP in colonic mucosa. These alterations are associated with malabsorption of sodium and chloride and could cause diarrhoea.

Animals↗
PubMed1981

Apneustic respiration normalized by an atypical cholinergic drug action in cats.

Cats were anesthetized with a mixture of pentobarbital and barbital given intraperitoneally and vagotomized. All animals were pretreated with atropine i.v. which blocked conventional muscarinic receptors and at the same time revealed atropine-insensitive sites whose stimulation by the cholinergic drug, bethanechol, was earlier found to produce respiratory analepsis. Respiration was recorded by pneumotachograph and intrapleural cannula. Apneustic breathing was produced by placing electrolytic lesions in the pneumotaxic area or by injecting a local anesthetic agent into the cerebrospinal fluid. Experiments were performed under isocapnic conditions. Bethanechol, administered intracerebro-ventricularly, restored regular breathing and increased the tidal volume in a dose-related manner within minutes of its injection. In cats with lesions, the expiratory pause generally decreased first and was followed by shortening of the inspiratory plateau. In cats made apneustic by intracerebro-ventricular injection of procaine, bethanechol acted competitively to normalize the distorted waveshape. The central excitant drug pentylenetetrazol was given intravenously for comparison with bethanechol. Apneustic breathing was partially corrected by pentylenetetrazol through a facilitatory influence on the brain stem interpreted to be independent of its convulsant action. These experiments demonstrate correction of pathological breathing by two chemically unrelated agents which share the ability to increase central excitatory state.

Animals↗
PubMed1989

Tracheal gland mucous cells stimulated in vitro with adrenergic and cholinergic drugs.

To determine the responsiveness of tracheal mucous cells to adrenergic and cholinergic stimulation, we analyzed changes in their structure induced by neurotransmitter-like agonists. Ferret tracheal rings were exposed for 30 min in vitro to one of the following: phenylephrine, isoproterenol, or bethanechol (all at 10(-5) M), in the presence of absence of appropriate antagonists. Electron microscopy and morphometric analysis revealed that the volume density of mucous cells (Vvmc, i.e. the space occupied by mucous cells in the submucosa) significantly decreased, and the surface density of mucous cell apical membrane (Svam) increased in response to isoproterenol and bethanechol but not to phenylephrine. In metabolic labeling experiments, the morphological changes were accompanied by secretagogue-evoked release of 35S-labeled macromolecules. Taken together, these data suggest that tracheal mucous cells secrete 35S-labeled macromolecules in response to beta-adrenergic and muscarinic agonists by an exocytotic process that involves a reduction in cell size.

Animals↗
PubMed1975

Cholinergic and adrenergic neuroreceptors in urinary tract of female dogs. Evaluation of function with pharmacodynamics.

Our preliminary pharmacodynamic studies on the lower urinary tract of adult female dogs indicate that cholinergic and adrenergic (alpha and beta) neuroreceptors in the urethra appear to coordinate the detrusor and urethral function during micturition. Urethral resistance measured as urethral pressure was easily altered with various pharmacologic agents. However, only bethanechol elicited detrusor response measured as intravesical pressure. The possible clinical usefulness of various drugs is outlined. Our results indicate the therapeutic value of ephedrine sulfate and propranolol in stress urinary incontinence; phenoxybenzamine in neurogenic vesical dysfunction and functional outlet obstruction; phenoxybenzamine plus bethanechol in atonic neurogenic bladder; and imipramine in enuresis.

Adrenergic alpha-Antagonists↗
PubMed1975

Effects of phenoxybenzamine hydrochloride on canine lower urinary tract: clinical implications.

The results of our study show that phenoxybenzamine hydrochloride, a potent long-acting alpha-adrenergic blocker, has clearly demonstrable effects on urethral function. In a dose of 0.5 mg. per kilogram of body weight it caused a significant lowering of the resting urethral pressure, a decrease in the arterial pressure, and no change in the intravesical pressure. Higher doses caused similar but more pronounced and prolonged effects. The combined use of phenoxybenzamine and bethanechol increased the intravesical pressure and decreased the urethral pressure. It appears that the predominant mechanism of urethral resistance is alpha-adrenergic activity in smooth muscle. A review of the medical literature, our experimental studies, and limited clinical application lead uo to conclude that phenoxybenzamine could be useful in treating neurogenic vesical dysfunction of various types, urethral syndrome, urgency incontinence, functional outlet obstruction with or without vesicoureteral reflux, drug-related obstructive urinary symptoms, partial prostatic obstruction, and ureteral colic. The combination of phenoxybenzamine and bethanechol could be used in managing patients with atony of the bladder of neuropathic or myopathic origin.

Adult↗