sincalide and asperlicin

sincalide has been researched along with asperlicin* in 7 studies

Reviews

1 review(s) available for sincalide and asperlicin

ArticleYear
[Cholecystokinin receptor antagonists].
    Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme, 1993, Volume: 38, Issue:11

    Topics: Amino Acid Sequence; Animals; Benzodiazepinones; Cholecystokinin; Furans; Indoles; Meglumine; Molecular Sequence Data; Proglumide; Receptors, Cholecystokinin; Sincalide; Thiophenes

1993

Other Studies

6 other study(ies) available for sincalide and asperlicin

ArticleYear
Partial agonism by gastrin for a cholecystokinin receptor mediating pepsinogen secretion.
    The American journal of physiology, 1993, Volume: 265, Issue:5 Pt 1

    Isolated gastric glands from rabbit were used to characterize the functional cholecystokinin (CCK)-like peptide receptors that mediate pepsinogen secretion. Pepsinogen secretion was stimulated by both CCK octapeptide sulfate (CCK-8) and A-71378, a selective CCK-A-type receptor agonist, with similar mean effective doses (1.0 and 0.8 nM, respectively). Compared with CCK-8, gastrin-17 (G-17-I) showed reduced potency and only partial efficacy for stimulation of pepsinogen secretion while inhibiting the maximal CCK-8-stimulated response. The nonpeptide inhibitors, asperlicin and L-364,718, inhibited pepsinogen secretion with identical pA2 values for antagonism of both CCK and gastrin, indicating that both peptides interact with the same functional receptor. Specific binding of [3H]CCK-8 to isolated chief cell membranes was displaced fully by both CCK and gastrin, indicating full receptor occupancy by both peptides. A novel synthetic peptide analogue, pseudogastrin [(Glu)5-Ala-Tyr-Nle-Gly-Trp-Nle-Asp-Phe-NH2], was used to investigate the structural basis for the lower potency and efficacy of G-17-I. The potency of CCK and gastrin analogues for pepsinogen secretion was found to be dependent on both sulfation of a tyrosine residue and the position of the tyrosine residue relative to the COOH-terminal phenylalanine amide. The efficacy appears to be determined partially by the extended NH2-terminal sequence of G-17-I. The results of the present study are interpreted to show that pepsinogen secretion is mediated by a CCK-A-type receptor and gastrin acts at the same receptor as a partial agonist.

    Topics: Amino Acid Sequence; Animals; Benzodiazepinones; Cell Membrane; Cholecystokinin; Devazepide; Gastric Mucosa; Gastrins; Hormones; In Vitro Techniques; Kinetics; Molecular Sequence Data; Oligopeptides; Pepsinogens; Rabbits; Receptors, Cholecystokinin; Sequence Homology, Amino Acid; Sincalide

1993
Involvement of different mechanisms in the stimulatory effects of cholecystokinin octapeptide on gastrointestinal and colonic motility in dogs.
    Canadian journal of physiology and pharmacology, 1989, Volume: 67, Issue:10

    The effects of an intravenous infusion of cholecystokinin octapeptide (CCK-8, 1 microgram.kg-1.h-1) were investigated in conscious fasted dogs chronically fitted with strain-gauge transducers on the antrum, the jejunum, and the colon. Attempts to antagonize the increase of motility appearing at the three levels during CCK infusion were made using different blockers to elucidate the mechanisms involved. Asperlicin (a specific CCK antagonist) blocked the effects of CCK-8 at the three levels, while atropine and somatostatin were only effective in the jejunum and colon. Methyl-levallorphan (a mu-opiate antagonist that poorly crosses the blood-brain barrier) antagonized the CCK-induced colonic stimulation when intracerebroventricularly administered. Serotonin, histamine, substance P, and K-antagonists as well as a benzodiazepine did not modify the CCK-8 induced stimulation. It was concluded that the stimulatory effect of CCK-8 resulted from (a) a direct stimulation of the smooth muscle cells at gastric level, (b) a cholinergic activation of the jejunum and the colon, and (c) the involvement of a mu-opioid central component in the colonic response only.

    Topics: Animals; Benzodiazepinones; Colon; Dogs; Female; Gastrointestinal Motility; Histamine Antagonists; Infusions, Intravenous; Injections, Intraventricular; Male; Narcotic Antagonists; Parasympatholytics; Serotonin Antagonists; Sincalide; Stimulation, Chemical

1989
The effect of cholecystokinin-octapeptide, insulin, glucagon, triiodothyronine, and epidermal growth factor on amylase activity in fetal pancreas in vitro.
    Pediatric research, 1988, Volume: 23, Issue:5

    To evaluate the possible role of various hormones on fetal pancreas development, late gestational fetal rat pancreata (20 days) were cultured in a serum-free medium for 6 days in the presence of cholecystokinin-octapeptide (CCK-8), epidermal growth factor, triiodothyronine, or glucagon with or without dexamethasone. In the absence of any added hormone, the tissue amylase activity declined very rapidly. Epidermal growth factor alone (4.10(-7) M) could not preserve the amylase activity, whereas triiodothyronine (0.1 microM) and glucagon (4 micrograms/ml) had a deleterious effect that was prevented by the addition of DXM (3.10(-6) M). In the presence of CCK-8 (2.10(-11) M) 50 and 30% of the amylase activity was maintained on the 2nd and the 4th day of culture, respectively. The CCK-8 effect was dose dependent and was inhibited by asperlicin (10 microM). The combination of CCK-8 and dexamethasone maintained more than 80% of the amylase activity in the fetal pancreas explants through 4 days of culture. Fetal pancreas cultured in this optimal medium and treated with streptozotocin (10(-7) M) during the 1st day of culture showed a significantly lower tissue amylase activity on the 4th and 6th days than those not treated with streptozotocin. The streptozotocin effect was attenuated when insulin (0.1 U/ml) was added. These data suggest that, in addition to the well-known effect of glucocorticoid on enzyme activities in the fetal pancreas, two additional hormones, CCK and insulin, could play a role in the modulation of pancreatic amylase activity in the fetal rat.

    Topics: Amylases; Animals; Benzodiazepinones; Cells, Cultured; Dexamethasone; Epidermal Growth Factor; Fetus; Gestational Age; Glucagon; Insulin; Pancreas; Rats; Rats, Inbred Strains; Sincalide; Streptozocin; Time Factors; Triiodothyronine

1988
Involvement of endogenous opiates in regulation of gastric emptying of fat test meals in mice.
    The American journal of physiology, 1988, Volume: 255, Issue:2 Pt 1

    The role of endogenous opioids and cholecystokinin (CCK) in gastric emptying was investigated in mice killed 30 min after gavage with 51Cr-radiolabeled liquid meals. The meals consisted of 0.5 ml of milk or one of five synthetic meals containing arabic gum, glucose and/or arachis oil and/or casein. Naloxone (0.1 mg/kg sc) significantly (P less than 0.01) accelerated gastric emptying of milk and meals containing fat but did not modify gastric emptying of nonfat meals. The CCK antagonist asperlicin (0.1 mg/kg ip) increased by 25% gastric emptying of milk. The gastric emptying of meals containing glucose and casein but not fat was reduced after administration of the COOH-terminal octapeptide of cholecystokinin (CCK-8, 4 micrograms/kg ip). This decrease was antagonized by both asperlicin (10 mg/kg ip) and naloxone (0.1 mg/kg sc). Intracerebroventricular (icv) administration of an opiate antagonist that poorly crosses the blood-brain barrier, methyl levallorphan (10 micrograms/kg), did not modify gastric emptying of milk but accelerated it when peripherally administered (0.1 mg/kg sc). Similarly, asperlicin (icv) administered at a dose of 1 mg/kg did not affect milk emptying. These results indicate that endogenous opiates are involved at peripheral levels in the regulation of gastric emptying of fat meals only and that such regulation involves release of CCK.

    Topics: Animals; Benzodiazepinones; Cholecystokinin; Chromium Radioisotopes; Dietary Fats; Endorphins; Gastric Emptying; Homeostasis; Male; Mice; Mice, Inbred Strains; Naloxone; Reference Values; Sincalide

1988
A new simple mouse model for the in vivo evaluation of cholecystokinin (CCK) antagonists: comparative potencies and durations of action of nonpeptide antagonists.
    Life sciences, 1986, Nov-03, Volume: 39, Issue:18

    A new simple mouse assay for the in vivo evaluation of CCK antagonists which is based upon visual determination of the gastric emptying of a charcoal meal is described. CCK-8 (24 micrograms/kg s.c.) but not various other peptide and nonpeptide agents effectively inhibited gastric emptying in this test system. The effect of CCK-8 was antagonized by established peripheral CCK antagonists but not representative agents of various other pharmacological classes. The rank order of potency of the CCK antagonists were: L-364,718 (ED50 = 0.01 mg/kg, i.v.; 0.04 mg/kg, p.o.) greater than Compound 16 (ED50 = 1.5 mg/kg, i.v.; 2.0 mg/kg p.o.) greater than asperlicin (ED50 = 14.8 mg/kg i.v.) greater than proglumide (ED50 = 184 mg/kg i.v.; 890 mg/kg, p.o.). Duration of action studies based upon ED50 values determined at various time intervals after oral administration showed that L-364,718 and proglumide are considerably longer acting than Compound 16. Asperlicin (ED50 greater than 300 mg/kg, p.o.) was ineffective as a CCK antagonist when administered orally. These data provide the first direct comparisons of the in vivo potencies of current CCK antagonists and demonstrate the utility of a new simple mouse assay for the in vivo characterization of peripheral CCK antagonists.

    Topics: Administration, Oral; Animals; Benzodiazepinones; Binding, Competitive; Cholecystokinin; Devazepide; Dose-Response Relationship, Drug; Female; Gastric Emptying; Mice; Proglumide; Sincalide; Time Factors

1986
Evidence that cholecystokinin octapeptide (CCK-8) acts as a potent, full agonist on gastrin receptors for acid secretion in the isolated mouse stomach: lack of antagonism by the specific CCK antagonist asperlicin.
    Digestion, 1986, Volume: 35, Issue:3

    Cholecystokinin octapeptide (CCK-8) (EC50 = 5 nM) was considerably more potent than pentagastrin (EC50 = 161 nM) in stimulating acid secretion in the isolated perfused mouse stomach suspended in a medium containing a phosphodiesterase inhibitor. The maximum acid response to CCK-8 was not significantly different from that produced by pentagastrin. The nonselective CCK/gastrin antagonist, proglumide, but not the selective CCK antagonist, asperlicin, antagonized the acid response to both pentagastrin and CCK-8. The data suggest that CCK-8 acts as a potent, full agonist on gastrin receptors for acid secretion in the isolated mouse stomach.

    Topics: Animals; Benzodiazepinones; Female; Gastric Acid; Gastric Mucosa; In Vitro Techniques; Mice; Pentagastrin; Receptors, Cholecystokinin; Sincalide

1986