sincalide and benzotript

sincalide has been researched along with benzotript* in 7 studies

Other Studies

7 other study(ies) available for sincalide and benzotript

ArticleYear
Gastrin stimulates Ca2+ mobilization and clonal growth in small cell lung cancer cells.
    Cancer research, 1992, Nov-01, Volume: 52, Issue:21

    Gastrin has been postulated to be a physiological growth factor, but compelling in vitro evidence of this has been difficult to obtain. In the present study we investigated whether small cell lung carcinoma cell lines could provide a useful model system to study the effects of gastrin on signal transduction and cell proliferation in vitro. We found that the addition of gastrin to small cell lung cancer cells loaded with the fluorescent Ca2+ indicator fura 2-tetraacetoxymethylester causes a rapid and transient increase in the intracellular concentration of Ca2+ ([Ca2+]i) followed by homologous desensitization. The [Ca2+]i response was especially prominent in the small cell lung carcinoma cell line H510. In this cell line, gastrin I, gastrin II, cholecystokinin residues 26-33 (CCK-8), and unsulfated CCK-8 increased [Ca2+]i in a concentration-dependent fashion with half-maximum effects at 7, 2.5, 3, and 5 nM, respectively. The Ca(2+)-mobilizing effects of gastrin and CCK-8 were prevented by proglumide, benzotript, and the specific gastrin/CCKB receptor antagonist L365260. Gastrin stimulated the clonal growth of H510 cells in semisolid (agarose-containing) medium, increasing both the number and the size of the colonies. Gastrin and CCK agonists were equally effective in promoting clonal growth. The broad-spectrum neuropeptide antagonists [D-Arg1,D-Phe5,D-Trp7,9,Leu11] substance P and [Arg6,D-Trp7,9,MePhe8] substance P (6-11) markedly inhibited gastrin-stimulated Ca2+ mobilization and clonal growth. These results show that gastrin acts as a direct growth factor through gastrin/CCKB receptors and demonstrate, for the first time, that these peptides can stimulate the proliferation of cells outside the gastrointestinal tract.

    Topics: Benzamides; Calcium; Carcinoma, Small Cell; Cell Division; Gastrins; Humans; Lung Neoplasms; Proglumide; Sincalide; Tumor Cells, Cultured

1992
The effect of cholecystokinin-receptor antagonists on cholecystokinin-stimulated bile flow in dogs.
    Surgery, 1991, Volume: 109, Issue:3 Pt 1

    Cholecystokinin is a choleretic in dogs. Some of the effects of cholecystokinin in stimulating bile flow in dogs are produced by cholecystokinin stimulating the release of other choleretic hormones such as insulin and glucagon. The purpose of this study was to determine the effects of cholecystokinin receptor antagonists on canine hepatic bile flow and insulin and glucagon release from the pancreas. Cholecystokinin octapeptide (CCK-8) and intraduodenal fat were administered to dogs that had undergone cholecystectomy with chronic biliary fistulas with and without the administration of cholecystokinin receptor antagonists. Bile secretion and systemic venous insulin, glucagon, and cholecystokinin levels were measured. The cholecystokinin receptor antagonists benzotript and CR 1409 had no effect on bile flow or hormone levels when administered without cholecystokinin, whereas proglumide produced a large increase in bile flow without altering hormone levels. The response produced by proglumide may be the result of an osmotic effect produced by the substance being secreted in bile and its stimulating bile salt secretion in bile. CCK-8 and intraduodenal fat increased bile flow, bile chloride secretion, and cholecystokinin, insulin, and glucagon concentrations in venous blood. The cholecystokinin receptor antagonists benzotript and CR 1409 significantly decreased the bile flow and insulin and glucagon changes produced by exogenous CCK-8. The effect of intraduodenal fat on bile flow was not inhibited by the cholecystokinin receptor antagonists, whereas the increased insulin and glucagon levels were decreased significantly. Intraduodenal fat may release other choleretic hormones not affected by cholecystokinin receptor antagonists. The choleresis produced by exogenous CCK-8 is inhibited by cholecystokinin receptor antagonists, perhaps by inhibiting the release of the choleretic hormones insulin and glucagon.

    Topics: Animals; Anti-Ulcer Agents; Benzamides; Bile; Bile Acids and Salts; Cholecystokinin; Corn Oil; Dogs; Electrolytes; Female; Glucagon; Insulin; Kinetics; Proglumide; Receptors, Cholecystokinin; Sincalide; Taurocholic Acid

1991
Cholecystokinin modulates neurotransmission through the dentate gyrus.
    Neuroscience letters, 1988, Dec-19, Volume: 95, Issue:1-3

    The sulfated and unsulfated cholecystokinin (CCK) octapeptide sequences and the pancreatic CCK antagonists, CR 1409 and benzotript, were administered iontophoretically while dentate gyrus granule cell activity was recorded in the anesthetized rat. During application of the compounds, the peri-stimulus time histogram (PSTH) was constructed of granule cell activity coupled to stimulation of the sciatic nerve. CCK and CR 1409, but not benzotript, were found to change significantly the PSTH by enhancing and prolonging the response to sensory stimulation. These results are interpreted as indicating that CCK can modulate impulse flow through the dentate gyrus.

    Topics: Action Potentials; Animals; Benzamides; Electric Stimulation; Hippocampus; Iontophoresis; Male; Proglumide; Rats; Rats, Inbred Strains; Sciatic Nerve; Sincalide; Synaptic Transmission

1988
The effects of cholecystokinin and cholecystokinin antagonists on synaptic function in the CA1 region of the rat hippocampal slice.
    Brain research, 1987, Jul-07, Volume: 415, Issue:1

    The effects of two CCK antagonists, benzotript and proglumide, and of sulfated and non-sulfated cholecystokinin octapeptide (CCK-8-S and CCK-8-NS), were studied in the CA1 region of the rat hippocampal slice. Both benzotript and proglumide shifted presynaptic volley (prevolley) vs population spike input/output (I/O) curves for Schaffer collateral-commissural synaptic transmission to the right. This result indicates that the antagonists had a net depressant effect on synaptic transmission. CCK-8-S shifted prevolley vs population spike I/O curves to the left, indicating a net excitatory effect. Analysis of component I/O curves indicated that CCK-8-S and the CCK antagonists were acting postsynaptically by changing CA1 pyramidal cell threshold. CCK-8-NS had no significant effect on overall or component I/O functions. These findings suggest that endogenous CCK is released, directly or indirectly, upon stimulation of the Schaffer collateral-commissural fibers and increases the excitability of CA1 pyramidal cells.

    Topics: Action Potentials; Animals; Benzamides; Female; Glutamine; Hippocampus; In Vitro Techniques; Proglumide; Rats; Rats, Inbred Strains; Sincalide; Sulfates; Synapses; Synaptic Transmission

1987
Intracerebroventricular injection of cholecystokinin octapeptide elevates plasma prolactin levels through stimulation of vasoactive intestinal polypeptide.
    Endocrinology, 1987, Volume: 121, Issue:1

    We investigated the effect of cholecystokinin octapeptide (CCK-8) on plasma PRL levels in freely moving male rats. Intravenous injection of CCK-8 did not affect basal plasma PRL levels in doses up to 5000 ng/rat; however, plasma PRL increased significantly after intracerebroventricular (icv) injection of the peptide at a dose of 40 ng/rat. Proglumide (0.2 mg/kg, iv) and benzotript (0.2 mg/kg, iv), specific CCK receptor antagonists, blocked the icv CCK-8-induced increase in plasma PRL levels. There was no apparent effect of icv CCK-8 on the enhancement of PRL release by haloperidol (0.2 mg/kg, iv), sulpiride (0.1 mg/kg, iv), domperidone (0.1 mg/kg, iv), or RO22-1319 (0.1 mg/kg, iv). However, the apomorphine-induced inhibition of PRL secretion was significantly antagonized by icv CCK-8. Furthermore, icv CCK-8 increased plasma PRL levels in rats depleted of dopamine by pretreatment with reserpine and alpha-methyl-p-tyrosine. Finally, the elevation in plasma PRL levels produced by icv CCK-8 was substantially antagonized by vasoactive intestinal polypeptide antiserum (1:3; 10 microliter/rat, icv). These results suggest that CCK-8 increases plasma PRL through an interaction with a central CCK receptor, which stimulates the activity of vasoactive intestinal polypeptide, a putative PRL-releasing factor.

    Topics: Animals; Apomorphine; Benzamides; Dopamine Antagonists; Immunosorbent Techniques; Injections, Intraventricular; Male; Proglumide; Prolactin; Rats; Rats, Inbred Strains; Sincalide; Vasoactive Intestinal Peptide

1987
Antagonists of central and peripheral behavioral actions of cholecystokinin octapeptide.
    The Journal of pharmacology and experimental therapeutics, 1986, Volume: 236, Issue:2

    Pharmacological studies on the behavioral functions of sulfated cholecystokinin (CCK) in the gut and in the brain require potent, specific antagonists to CCK. Compounds identified as competitive antagonists at the peripheral receptors for CCK were tested for their ability to block the behavioral effects of CCK administered centrally and peripherally. Behavioral effects of CCK (8.8 X 10-10 mmol) administered centrally into the nucleus accumbens, i.e., potentiation of dopamine-induced hyperlocomotion in rats, were effectively blocked by pretreatment with proglumide (6 X 10(-5) mmol of nucleus accumbens), by benzotript (3 X 10(-5) mmol of nucleus accumbens) and by rabbit antiserum raised against CCK (0.2 microliter/nucleus accumbens), but not by CCK26-33 (1.7 X 10(-7) mmol) or unsulfated CCK26-33 (1.9 X 10(-6) mmol). The behavioral effects of peripherally administered CCK, i.e. reduced food consumption and reduced exploratory behaviors in mice, were blocked effectively by pretreatment with proglumide (0.3-0.9 mmol/kg), and by benzotript (0.03 mmol/kg), but not by CCK30-33 (0.003 mmol/kg). None of the compounds administered peripherally significantly affected food consumption or exploratory behaviors when given alone. Furthermore, none of the compounds significantly affected locomotion when administered alone into the nucleus accumbens, or significantly affected dopamine-induced hyperlocomotion when given into the nucleus accumbens before dopamine. Benzotript, proglumide and a CCK antibody appear to act as specific antagonists of the behavioral effects of CCK at both the peripheral gastrointestinal site and at the central nucleus accumbens site. Neither unsulfated CCK26-33 or CCK30-33 were effective as antagonists of peripheral or central behavioral effects of CCK. However, whereas benzotript and proglumide may be useful as pharmacologically specific antagonists, the high doses required suggest that more potent CCK antagonists are required for investigating the behavioral functions of endogenous CCK.

    Topics: Animals; Behavior, Animal; Benzamides; Brain; Dopamine; Dose-Response Relationship, Drug; Eating; Exploratory Behavior; Immune Sera; Male; Mice; Motor Activity; Nucleus Accumbens; Proglumide; Rats; Rats, Inbred Strains; Receptors, Cell Surface; Receptors, Cholecystokinin; Sincalide

1986
Differentiation of central and peripheral cholecystokinin receptors by new glutaramic acid derivatives with cholecystokinin-antagonistic activity.
    Arzneimittel-Forschung, 1986, Volume: 36, Issue:1

    Three glutaramic acid derivatives provided with a potent antagonistic activity on the contractions elicited by the carboxyl terminal octapeptide CCK-8 in the guinea pig gallbladder have been evaluated for their capacity to inhibit the binding of [125I]-(Bolton-Hunter)-CCK-8 to both central and peripheric cholecystokinin (CCK) receptors. The most active compound inhibits the CCK binding to rat pancreas acini at a concentration 10(-7) mol/l, but only at 10(-4) mol/l on cerebral cortex membranes, confirming the existence of at least two different populations of CCK receptors.

    Topics: Animals; Benzamides; Cerebral Cortex; In Vitro Techniques; Kinetics; Male; Mice; Pancreas; Proglumide; Rats; Receptors, Cell Surface; Receptors, Cholecystokinin; Sincalide; Tetragastrin

1986