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At least 793 records · Page 44Linked to original sources
PubMed1994

Comparative pharmacology of the male and female rabbit bladder neck and urethra: involvement of nitric oxide.

The present study compared the contractile and relaxant responses of male and female rabbit bladder neck and urethra to field stimulation (FS) and various contractile and relaxant agents, with special attention paid to the involvement of nitric oxide (NO) in the mediation of field-stimulated relaxation. FS at basal tension elicited a frequency-dependent contractile response in all preparations. The maximal response to high frequency FS was significantly greater in the bladder neck strips isolated from male rabbits than in those from female rabbits. There were no significant differences in the response to bethanechol or phenylephrine between strips isolated from males and females. Field-stimulated responses of the strips from male bladder neck and urethra were greater than the response to phenylephrine. The responses of all strips to FS were greater than those to bethanechol. In addition, the response to phenylephrine was generally greater than that to bethanechol. Phentolamine was a significantly more effective inhibitor of the response of the female bladder neck and urethral strips to FS than of the response of the male strips. The contractile response of all strips to phenylephrine was generally greater than that to bethanechol for both sexes and for both bladder neck and urethral strips. NG-nitro-L-arginine methylester (L-NAME) inhibited totally the field-stimulated relaxation of all strips. Isoproterenol stimulated a slowly developing but significant inhibition of phenylephrine prestimulated contractions. In conclusion, significant differences exist in the magnitude of field-stimulated relaxation between the bladder neck and urethra of both male and female rabbits, and, for all tissues, field-stimulated relaxation could be completely inhibited by pretreatment with L-NAME, an NO synthesis inhibitor.

Animals↗
PubMed1992

Secretion mode of the harderian gland of rats after stimulation by cholinergic secretagogues.

We studied the morphological changes in rat Harderian glands 30 min after injection of cholinergic secretagogues. In controls, the glands exhibited a tubuloalveolar structure with relatively wide lumina, in which some osmiophilic dense droplets exocytosed from glandular cells were observed. Also two types of glandular cells (type A cells and type B cells sometimes showing exocytotic figures of lipid-secretory vacuoles) and myoepithelial cells were recognized. After injection of carbamylcholine chloride (subcutaneously, 0.1 mg/kg body weight), which has both nicotinic and muscarinic actions, many of the alveolar lumina dilated and contained a small number of osmiophilic droplets. Exocytotic figures in both types of cells and a pronounced decrease in the number of vacuoles in the glandular cells were observed. However, there was no evidence of apocrine or holocrine secretion. The injection of the higher dose of carbamylcholine (1.0 mg/kg) caused fusion of secretory vacuoles in the apical cytoplasm and contraction of myoepithelial cells. Most alveoli showed no clear lumina; their centers were jammed with cytoplasmic fragments and accumulated secretory products. Massive discharge of cytoplasmic fragments containing some secretory vacuoles was often observed. This may be classified as apocrine secretion. Bethanechol chloride (subcutaneous injection, 1.0 mg/kg), a muscarinic agonist, stimulated the Harderian-gland secretion, and enhanced exocytosis was observed. The discharge from the glandular cells, following injection of various doses of carbamylcholine, were almost inhibited by atropine sulfate, a muscarinic antagonist. The present results suggested that the cholinergic systems regulate the secretion of rat Harderian-gland cells which have muscarinic receptors.

Animals↗
PubMed1976

Gastric secretory response to cholinergic stimulation in rats chronically pretreated with pentagastrin or histamine in depot form.

Rats pretreated by daily depot injections of pentagastric for 24 days, responded with a significant increase of gastric secretion volume, and HC1 concentration and output, when infused intravenously with bethanechol chloride. In these rats, the total weight of the stomach and the height of the fundic mucosa were also increased. Pretreatment with histamine had no effect on rat gastric tissue or gastric secretion, under identical conditions of stimulation.

Animals↗
PubMedDate not supplied

Effect of early weaning of the neonatal rat on pancreatic acinar cell responsiveness to urecholine.

Pancreatic response to urecholine was studied in rats weaned prematurely on the morning of their 13th, 15th, 17th and 19th day and killed 2 1/2 days later. In pups kept with their mother and weaned at 21 days, amylase chymotrypsin and lipase concentrations increased gradually. Weaning after 12, 14 and 16 complete days is associated with significant increases in pancreatic amylase and chymotrypsin concentrations; if it occurs after 16 and 18 days, a significant delay in lipase development is observed. Premature weaning is associated with modifications in the basal release of the three enzymes and their secretion in response to urecholine. Amylase and chymotrypsin secretions are increased if weaning occurred before day 18. Lipase secretion, however, is decreased in rats weaned after 16 days. If, however, secretion is expressed in percentages, as the amount of enzyme released over the total tissue content, premature weaning does not seem to modify the capacity of the tissue to secrete enzymes under basal and urecholine stimulation. It thus seems that solid food intake as early as 12 days is not an important factor in the maturation of the pancreatic response to urecholine.

Amylases↗
PubMed1978

Delayed weaning and denial of solid food nibbling upon pancreatic acinar cell responsiveness to urecholine in neonatal rats.

Pancreatic response to urecholine was studied in rats which were fed maternal milk only until they reached 27 days of age. A group of pups which remained all the time with their mother were weaned at 21 days; over that nursing period, their pancreatic amylase concentration increased gradually, lipase started to decrease from day 23 while chymotrypsin remained constant. In those who were denied solid food from day 12, the amylase concentration fell significantly from day 23 to 27 while lipase and chymotrypsin rose rapidly. Delayed weaning was associated with significant decreases in basal and urecholine-stimulated amylase secretion from day 23, whereas lipase and chymotrypsin releases were increased. If, however, secretion is expressed in percentages of the amount of enzyme released over the total tissue content, the output of the three enzymes in response to urecholine is significantly reduced from day 25 in pups kept on maternal milk only. These results suggest that dietary fat and carbohydrate modulate the enzyme content of the pancreas and that milk as the only source of energy and protein reduces the pancreatic acinar cell responsiveness to urecholine.

Amylases↗
PubMed1982

Acid and pepsin secretion in chronic Chagas' disease patients in response to graded doses of pentagastrin and pentagastrin plus bethanecol.

Gastric acid and pepsin secretory responses to graded doses of pentagastrin were measured in 12 Chagas' disease patients and 18 control subjects, and in 7 Chagas' disease patients and 6 controls the study was repeated with an infusion of bethanecol. Calculated maximal outputs of acid and pepsin (Vmax) and responsiveness (D50) of the acid- and pepsin-secreting cells to pentagastrin were lower in the chagasics. Bethanecol had no significant effect on pentagastrin-stimulated gastric secretions in controls. The impairment of responsiveness of the gastric secretory cells in Chagas' disease patients was fully corrected by bethanecol.

Adolescent↗
PubMed1983

Calcium secretion from the feline pancreas. Influence of hormonal and cholinergic secretagogues and of serum calcium.

The influences of secretagogues and of elevated serum calcium concentrations on the calcium secretion from the cat pancreas have been studied in vivo. During a high and constant fluid secretion rate evoked by a background infusion of secretin, additional infusions of both cholecystokinin-pancreozymin and urecholine led to a dose-dependent increase in calcium secretion in pancreatic juice parallel to the rise of protein. The amount of calcium in pancreatic juice associated to 1 mg protein (18.3 nmol/mg protein) calculated from regression analysis was independent of dose or kind of stimulus used. The protein-independent pancreatic juice calcium fraction was 0.184 mM in normocalcemia. During an episode of hypercalcemia produced by an intravenous calcium infusion, the protein-independent calcium fraction was increased and correlated linearly to the serum calcium concentration. We conclude that pancreatic juice calcium consists of two major fractions, one being associated with the enzyme protein and stimulated by secretagogues, and the other being protein independent and directly dependent on the extracellular calcium concentration.

Animals↗
PubMed1985

Medical management of reflux esophagitis.

Esophageal reflux should be treated only if symptoms are severe enough for patients to seek therapy or if esophagitis results. One study found that the number of reflux episodes lasting more than 5 min was the best indicator of esophagitis. Factors such as efficiency of the antireflux barrier, esophageal clearing, and aggressive power of refluxed material impact on the pathogenesis of reflux esophagitis. Therapy should be aimed at these factors and depends on severity of disease. Dietary measures, postural measures, and drug therapy can be used to alleviate symptoms and/or improve healing of esophageal lesions, with surgery recommended only in rare cases. Antacids, Gaviscon, and motor-stimulating drugs (metoclopramide, domperidone, bethanechol) may be sufficient to treat pathologic reflux without esophagitis. Once erosive or ulcerative lesions have developed, more rigorous medical treatment including H2 receptor blockers is mandatory.

Antacids↗
PubMed1987

Effects of pirenzepine and atropine on amylase response to various secretagogues from the rat pancreatic acini.

CCK-8, bombesin, secretin and urecholine added in various concentrations to the incubation medium of the dispersed pancreatic acini, obtained from rats, resulted in a dose-dependent stimulation of amylase secretion, the half-maximal response being achieved at 3 X 10(-12), 10(-10), 10(-7) and 10(-5) M, respectively. Pirenzepine (selective muscarinic M1 receptor blocker) or atropine failed to affect the amylase responses to all these secretagogues except that to urecholine, which was reduced by both antimuscarinic agents. The inhibition of urecholine-induced half-maximal amylase secretion by both anticholinergics was concentration-dependent, and the inhibitory potency of pirenzepine was about 1,000 times lower than that of atropine.

Amylases↗
PubMed1989

Exaggeration of the cholecystokinin-induced motor response in the cat gastrointestinal tract.

A stimulation of distal colonic motor activity was produced in anesthetized cats following intravenous administration of cholecystokinin. The contractile response elicited by cholecystokinin was not reduced following pretreatment with atropine. However, when animals were treated with agents which increased the net cholinergic input to the colon, a marked exaggeration of the subsequent cholecystokinin-induced response occurred. This cholinergically mediated exaggeration was produced following administration of the cholinergic agonist bethanechol, or after removal of tonic inhibitory systems mediated by prostaglandin or alpha-adrenergic input, whose blockade results in atropine-sensitive colonic stimulation. Cholecystokinin was also found to produce stimulation of motor activity in the pylorus, jejunum, proximal colon and gallbladder. Cholinergically mediated exaggeration of the cholecystokinin response was also present in the pylorus and proximal colon, but not gallbladder or jejunum. An inhibition of spontaneous motor activity was produced in the ileum or duodenum following cholecystokinin administration.

Animals↗
PubMed1989

Comparison of telenzepine, pirenzepine and atropine on gastric acid and pepsin secretion in response to histamine, pentagastrin, bethanechol, sham-feeding and feeding.

This study was designed to compare gastric antisecretory effects of telenzepine, a new antimuscarinic agent, with those of pirenzepine and atropine in dogs. None of these antimuscarinics affected gastric acid secretion induced by histamine but all of them caused a dose-dependent inhibition of acid secretion from the gastric fistula (GF) and Heidenhain pouches (HP) stimulated by pentagastrin and bethanechol, telenzepine being 5-9 times more potent than pirenzepine and equipotent with atropine. All antimuscarinics were also effective inhibitors of acid responses to sham feeding and ordinary feeding. The inhibitory effect of telenzepine and pirenzepine were not accompanied by any major alterations in plasma gastrin or somatostatin but those of atropine were related to significant increase in plasma gastrin and to significant decrease in plasma somatostatin levels, suggesting the involvement of M2 receptors in the cholinergic control of these hormones. All three antimuscarinics were effective inhibitors of pepsin secretion induced both from the GF and HP by all secretagogues used. Neither telenzepine nor pirenzepine administered in various doses affected the heart rate while atropine caused a significant increase in heart rate confirming that the former agents are selective M1 receptor antagonists. This study provides evidence that telenzepine is more potent than pirenzepine in the inhibition of gastric secretion induced by pentagastrin, bethanechol, sham-feeding and ordinary feeding and that, unlike atropine, it does not increase plasma gastrin responses to meat feeding. In fact, telenzepine and pirenzepine alike reduced plasma gastrin concentrations under these conditions. No influence of these antimuscarinics on plasma somatostatin levels was observed.

Animals↗
PubMed1992

Gastric antisecretory effects of esaprazole in rats.

The effects of esaprazole on gastric secretion (volume, pepsin and acid output) were investigated on animal models, both in vivo and in vitro. In conscious rats whose vagal activity was stimulated by pylorus ligation, esaprazole decreased volume, acid output and pepsin secretion. In anaesthetized stomach-perfused rats, esaprazole inhibited gastric acid secretion evoked by both vagus nerve stimulation or bethanechol infusion. By contrast, on isolated guinea-pig gastric fundus, esaprazole failed to counteract the acid output stimulated by histamine, bethanechol or pentagastrin. In addition to this, phasic contractions evoked by acetylcholine on isolated guinea-pig ileum were antagonized by esaprazole only at high concentrations. The present results suggest that the inhibitory actions of esaprazole on secretory parameters involve the cholinergic parasympathetic pathway, probably through both direct and indirect mechanisms.

Acetylcholine↗
PubMed1993

Adenosine and cholinergic-induced gastric contraction in rats.

Adenosine is known for its modulatory effects on gastric secretory function and mucosal blood flow in rats. However, its action on gastric motility has not been defined. The influence of adenosine on gastric contractions provoked by cholinergic drugs and direct vagal stimulation have, therefore, been examined. Bethanechol (25, 50 or 100 micrograms/kg i.v.) and electrical vagal stimulation dose and voltage dependently increased the number and the amplitude of gastric contractions. An adenosine-A1-receptor agonist, L-phenylisopropyladenosine (10 or 50 micrograms/kg s.c.), given 30 min beforehand, did not affect the changes in gastric parameters but decreased the basal mean blood pressure and lessened the reduction in blood pressure evoked by bethanechol. The adenosine-A2-receptor agonist N-ethylcarboxaminoadenosine (1 or 5 micrograms/kg s.c.), 30 min beforehand, however, significantly increased the number but not the force of gastric contractions; a lower dose of this drug increased the basal blood pressure and potentiated the depressive action of bethanechol on systemic blood pressure. Adenosine administration (7.5 mg/kg s.c.) significantly increased its plasma levels at 30 and 60 min after injection; pretreatment with it (2.5, 7.5 or 12.5 mg/kg s.c.), 30 min beforehand, did not affect the gastric and vascular actions of bethanechol. The highest dose of adenosine potentiated the contractile response of vagal stimulation. In the isolated fundus preparation, adenosine added to the organ bath (10(-6), 10(-4), 10(-2) M) also did not affect the contractions induced by acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1986

Selective effect of nortriptyline on smooth muscle as an anticholinergic drug: a pharmacological and clinical study.

The anticholinergic potency of nortriptyline was studied on muscle strips from human bladder and ileum. Concurrently the effect of nortriptyline low dosage therapy was studied in 21 women suffering from motor or sensory urgency and urge incontinence. Analysis of the results by the dose ratio method showed a significant difference in the affinity of the anticholinergic receptors to the antagonist. The Ki values were 0.298 microM for the bladder and 0.938 microM for the ileum. In the clinical study, the condition of 15 (71.4%) women treated with notriptyline improved considerably. The higher affinity of the drug to the receptors in the bladder than to those in the ileum may explain the positive therapeutic effect of a relatively low dose of nortriptyline in over 70% of the patients treated.

Bethanechol Compounds↗
PubMed1992

The development of polyanhydrides for drug delivery applications.

This paper reviews the development of the polyanhydrides as bioerodible polymers for drug delivery applications. The topics include design and synthesis of the polymer, physical properties, techniques to fabricate the polymer into drug delivery devices, evaluation of biocompatibility, and example applications of the polyanhydrides. Discussion of the interrelationship between the physical-chemical properties of the polyanhydrides, fabrication methods, and drug release rates is included. One section is devoted to a case study to provide a historical perspective of the development a polyanhydride-based drug delivery treatment from the conception of the idea to the final stages of human clinical trials. This section includes an outline of the extensive in vitro and in vivo testing that is necessary for development of a new material for biomedical applications.

Alzheimer Disease↗