Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sheep which had been either previously infected with 3. circumcincta or maintained worm-free, were surgically prepared with separated fundic pouches and abomasal cannulae and subsequently infected with 20,000 O. circumcincta larvae three times weekly. A reduction in food intake and increases in total acid output from the pouches and plasma pepsinogen levels were evident in both groups of sheep 4 days after repeated infections commenced; effects which increased in severity after 12 or more days. Except for a transient period of slight failure, previously infected sheep retained the capacity to acidify their abomasal contents whereas previously worm-free sheep lost this capacity. These changes were reversed between 2 and 7 days after treatment with thiabendazole (88 mg.kg-1). Secretory capacity of the fundic pouches was tested with histamine (40 mug.kg-1), the histamine antagonist (burimamide 8 mg.kg-1) and atropine (100 mug.kg-1). Ostertagiasis reduced or abolished the stimulatory effects of histamine. An increase in secretion volume and acid output was obtained after food was freshly provided, even though as little as 25 gm was consumed. Atropine and burimamide both caused a profound decrease in pouch secretion and acid output. These data are consistent with the hypothesis previously stated that in ostertagiasis the hypersecretion from fundic pouches is due to increased levels of circulating gastrin.
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PMID:Effects of a series of infections of Ostertagia circumcincta on gastric secretion of sheep. 125 6

Frog esophageal mucosa contains peptide glands which release pepsinogen in response to a variety of secretagogues and serves as a model to examine the inhibitory action of somatostatin. The pepsinogen secretion in response to bethanechol was inhibited by somatostatin in a noncompetitive fashion. The maximal response induced by bethanechol was reduced and the EC50 for bethanechol was increased in the presence of somatostatin. On the other hand, somatostatin showed essentially no effect on pepsinogen release evoked by ionophore A23187, dibutyryl cAMP or by forskolin in the presence of atropine. Atropine was included in the incubation mixture to eliminate the effect of acetylcholine released by forskolin from the intrinsic cholinergic neurons also present in the mucosa. Somatostatin did not exert any significant effect on the basal or the forskolin-stimulated cAMP accumulation in the mucosa, nor the basal or the forskolin-stimulated adenylate cyclase activity in the membranes of the peptic cells isolated from the mucosa. Thus, these results seem to suggest that somatostatin inhibits pepsinogen secretion from frog esophageal mucosa by a cAMP-independent pathway.
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PMID:Somatostatin inhibits pepsinogen secretion via a cyclic AMP-independent pathway. 167 98

Carbachol and secretions from Ostertagia species parasites significantly (P less than 0.001) stimulated isolated preparations of dispersed gastric glands from bovine and ovine abomasal mucosa to secrete pepsinogen. Atropine reduced the response to both secretagogues. Live adult and larval stages of Ostertagia ostertagi and O circumcincta and homogenates of these parasites did not significantly (P greater than 0.05) increase pepsinogen production from bovine or ovine gland preparations.
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PMID:Stimulated pepsinogen secretion from dispersed abomasal glands exposed to Ostertagia species secretion. 230 Jul 18

Although cholecystokinin (CCK) has been reported to stimulate pepsinogen secretion, this action has been poorly characterized. To assess the ability of CCK to regulate mammalian pepsinogen secretion, guinea pig fundic mucosa was incubated in Ussing chambers with CCK-8, carbamylcholine, and pentagastrin, and with cholinergic and CCK antagonists. CCK-8 stimulated pepsinogen secretion at 10(-10) M, with an ED50 of 10(-9) M and maximally (26-fold over basal) at 10(-8) M. Carbachol stimulated pepsinogen and acid secretion with an ED50 of 3 x 10(-7) M and maximally at 10(-6) M. Pentagastrin (10(-9) M-10(-6) M) did not affect acid or pepsinogen secretion, whereas gastrin-I (10(-6) M) stimulated acid secretion slightly but did not alter pepsinogen secretion. L364, 718 (10(-5) M), a specific CCK peripheral receptor antagonist, abolished all pepsigogic effects of 3 x 10(-9) M CCK-8 without altering basal acid or pepsinogen secretion or mucosal electric characteristics. L364,718-treated tissues unresponsive to CCK-8 nevertheless secreted pepsinogen and acid in response to 3 x 10(-7) M carbachol identically to control carbachol-treated preparations. Atropine (10(-5) M) blocked the response to 3 x 10(-7) M carbachol without inhibiting 10(-9) M CCK stimulation. These results support a specific receptor-mediated role for cholecystokinin in the physiologic regulation of guinea pig pepsinogen secretion.
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PMID:Effects of cholecystokinin and cholinergic receptor blockade on guinea pig pepsinogen secretion. 240 88

The in vitro release of pepsinogen secretion by the isolated esophagus of the American bullfrog was studied with an improved model system. The tissue was mounted in a double chamber that preserves mucosal polarity and provides both control and test segments, each 1 cm2 from the same tissue. Pepsinogen secretion was severalfold higher than previously found with mucosal strips and could be sustained for several hours. Bethanechol (BCh) caused concentration-dependent (0.1-50 microM) pepsinogen secretion with a Vmax of 74 +/- 12 micrograms X mg prot-1 X h-1 or 50-60% of total pepsinogen; Km was 3 microM and 500 microM BCh stimulated at less than the Vmax value. Atropine specifically blocked BCh and pA2 = 9.3. In the presence of 100 microM isobutylmethyxanthine, BCh produced a dose-dependent increase in tissue cAMP but not cGMP. BCh remained effective in Ca2+-free medium. In calcium-free medium EGTA concentration dependently (0.2-5 mM) suppressed the pepsinogen response to BCh. The evidence thus far suggests that cholinergic stimulation of pepsinogen secretion in the tissue acts via both cAMP and Ca2+. More specific studies would be required for absolute confirmation of either or both apparent mechanisms and to resolve how they interact.
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PMID:Mediation of muscarinic stimulation of pepsinogen secretion in the frog. 257 56

The muscarinic receptors coupled to pepsinogen secretion on isolated frog esophageal peptic cells have been characterized using functional and radioligand binding techniques. N-[3H]methylscopolamine [( 3H]NMS) binding to intact cells was complex and indicative of a high affinity, low capacity site and a high capacity uptake site. Binding to the high capacity site was inhibited by atropine with high affinity (IC50, 3 nM) and by imipramine and propranolol with IC50 values of 70 and 270 nM, respectively. After inhibition of uptake by 30 microM propranolol, [3H]NMS bound to a single population of high affinity sites (KD, 125 +/- 16 pM), which exhibited binding site maximum of 2.1 fmol/10(6) cells, equivalent to 1260 sites/cell. Binding to these sites was reversible, stereoselective and inhibited by muscarinic receptor agonists with an order of potency: oxotremorine greater than acetylcholine greater than carbachol greater than bethanechol and by antagonists with an order of potency:atropine greater than 4-diphenylacetoxy-N-methylpiperidine methobromide greater than pirenzepine greater than AF-DX 116 (11-2[2-[[diethylamino) methyl]-1-piperidinyl]acetyl]-5, 11-dihydro-6H-pyrido[2,3-b][1,4]-benzodiazepine-6-one). Pepsinogen secretion was stimulated by the agonists with an order of potency: acetylcholine greater than or equal to carbachol greater than oxotremorine greater than bethanechol. Atropine, pirenzepine and AF-DX 116 competitively inhibited carbachol-stimulated pepsinogen secretion with pA2 values of 9.58, 7.37 and 6.68, respectively, which correlated with their log (inhibition constants) for receptor binding. By contrast, agonists with significant efficacy exhibited EC50 values which were 20 to 90 times lower than their inhibition constants for binding which suggests the possibility of "spare" muscarinic receptors. Our findings indicate that functional muscarinic receptors on peptic cells exhibit similar characteristics to the high affinity sites labeled by [3H]NMS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscarinic cholinergic receptor subtype on frog esophageal peptic cells: binding and secretion studies. 290 89

In order to define the early transient responses of peptic cells to stimulation, we have modified the acidified hemoglobin substrate digestion method for pepsin to provide a very sensitive, linear (10-250 ng/ml), reproducible, inexpensive (less than 3 cents/sample) and simple semi-automated assay. Using a specially designed perifusion chamber, this method was used to accurately measure secretion at 1 min intervals from approximately 3 mg of isolated peptic glands from the esophageal peptic organ of R. catesbeiana, containing approximately 150 micrograms pepsinogen. Responses to carbachol applied for 1, 2 and 4 min could be described in discrete 1 min intervals. Secretion stimulated by carbachol (1-2 min) peaked at 200-300% of basal and upon withdrawal decayed with t1/2 approximately 3 min. Atropine added to continuous carbachol stimulation inhibited secretion with t1/2 approximately 4 min, indicating rapid metabolism of activated messengers.
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PMID:Pepsinogen secretion from perifused frog peptic glands: rapid transients detected with a modified pepsin assay. 312 74

We studied the effects of the neuropeptide gastrin-releasing peptide on pepsinogen secretion using an isolated perfused rat stomach with intact vagal innervation. Following electrical stimulation of the vagus nerves, the pepsin output to the luminal effluent increased from 94 +/- 7 to 182 +/- 24 units pepsin/min and the release of immunoreactive gastrin-releasing peptide to the venous effluent increased from 0.059 +/- 0.014 to 0.138 +/- 0.028 pmol/min. Infusion of gastrin-releasing peptide at 10(-8) M significantly increased pepsin output (from 87 +/- 17 to 129 +/- 22 units pepsin/min) and simultaneous infusion of gastrin-releasing peptide and carbachol at 10(-8) and 10(-6) M, respectively, resulted in an increase to almost 4 times the basal values. Atropine reduced but did not abolish the pepsin response to vagal stimulation and to infusion of gastrin-releasing peptide. Our results suggest that gastrin-releasing peptide participates in the vagal control of pepsinogen secretion.
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PMID:Role of gastrin-releasing peptide in pepsinogen secretion from the isolated perfused rat stomach. 314 68

Acid and pepsinogen secretion were studied in the isolated luminally perfused mouse stomach. Stimulation was obtained with bethanechol 10(-5)M. Pirenzepine blocked the effect of bethanechol in a dose dependent manner. The minimal blocking dose was 10(-5)M. Atropine 10(-6)M blocked secretion to a similar extent as pirenzepine 10(-5)M. Addition of tetrodotoxin did not change the response to bethanechol or to bethanechol together with pirenzepine. It is concluded that acid and pepsinogen secretion stimulated by bethanechol are inhibited by atropine and pirenzepine. There is at present no evidence that bethanechol stimulation or antimuscarinic inhibition act via intramural nerves.
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PMID:Pirenzepine inhibits acid and pepsinogen secretion by the isolated perfused mouse stomach. 612 94

To study the regulation of pepsinogen secretion by chief cells, we have developed techniques for the isolation, enrichment, and short-term culture of chief cells from canine stomach. The fundic mucosa was enzyme dispersed and chief cells were enriched to a content of about 70% using an elutriator rotor. After 36 h in culture confluent monolayers formed that were highly enriched in chief cells. Carbachol induced a time-dependent release of pepsinogen into the medium, with about a threefold increase in pepsinogen secretion over controls found after 60 min of incubation. Carbachol stimulation of pepsinogen secretion was dose dependent, with 5 microM producing 50% of the maximal response found at a carbachol concentration of 100 microM. Atropine (100 microM) produced a rightward shift of the dose-response curve, indicating the presence of a muscarinic receptor. Dibutyryl cAMP, 8-bromo-cAMP, and forskolin also markedly stimulated pepsinogen secretion. Secretin and vasoactive intestinal peptide (VIP) stimulated pepsinogen secretion, but the response were of smaller magnitude than found with carbachol or the cAMP analogues. The phosphodiesterase inhibitor isobutylmethylxanthine also caused a small stimulation of pepsinogen secretion but did not enhance the response to secretin or VIP. These findings indicate that epithelial monolayers can spontaneously form from isolated canine chief cells and retain functional differentiation evident by a response to stimulation. Canine chief cells in culture possess muscarinic and secretin receptors and respond to cAMP.
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PMID:Regulation of pepsinogen release from canine chief cells in primary monolayer culture. 619 27


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