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PubMed1998

Serotonin and cholecystokinin activate different populations of rat mesenteric vagal afferents.

This electrophysiological study was performed to elucidate the interactions of serotonin (5-hydroxytryptamine, 5-HT) and cholecystokinin (CCK) on mesenteric afferents supplying the rat jejunum. 5-HT and CCK produced characteristic responses in multi-unit recordings of mesenteric afferents. Waveform analysis to extract single units from the whole nerve recording identified populations of single afferents that were sensitive to either 5-HT or CCK, but not both. Furthermore, devazepide (0.5 mg/kg) completely abolished the response to CCK without altering the response to 5-HT while granisetron (0.5 mg/kg) abolished the response to 5-HT with no effect on the response to CCK. These results suggest that there are discrete, noninteractive populations of jejunal afferents that possess either 5-HT3 or CCK-A receptors but not both.

Animals↗
PubMed1999

Cholecystokinin receptor agonists block the jumping behaviour precipitated in morphine-dependent mice by naloxone.

The aim of present study was to reveal the role of cholecystokinin (CCK) in the jumping behaviour induced by the opioid antagonist naloxone (30 mg/kg) after the acute administration of morphine (200 mg/kg) in mice. Treatment with caerulein (0.01-1 microg/kg), a nonselective agonist of CCK receptors, induced a large reduction of jumping frequency without parallel suppression of locomotor activity. The CCK(B) receptor agonist CCK tetrapeptide (CCK-4. 0.125-32 mg/kg) caused the same effect, but it happened at much higher doses (above 0.5 mg/kg). Devazepide (1 microg/kg), a preferential CCK(A) receptor antagonist, completely reversed the action of caerulein (0.1 gmg/kg) and CCK-4 (2 mg/kg). A preferential CCK(B) receptor antagonists LY 288,513 at a high dose (4 mg/kg) blocked the action of CCK-4, but not that of caerulein. Acetorphan (16-128 mg/kg), an inhibitor of enkephalin metabolism, did not block naloxone-precipitated jumping behaviour. However, the combination of subthreshold doses of caerulein (0.001 microg/kg) and CCK-4 (0.25 mg/kg) with acetorphan (64 mg/kg) potently antagonized the behaviour induced by naloxone. In conclusion, the antagonism of CCK agonists against naloxone-precipitated jumping behaviour is apparently mediated via the CCK(A) receptor subtype. The stimulation of CCK(A) receptors seems to increase the release of endogenous enkephalins.

Animals↗
PubMed1997

Synthesis and stereochemical structure-activity relationships of 1,3-dioxoperhydropyrido[1,2-c]pyrimidine derivatives: potent and selective cholecystokinin-A receptor antagonists.

The synthesis and stereochemical structure--activity relationships of a new class of potent and selective non-peptide cholecystokinin-A (CCK-A) receptor antagonists based on the 1,3-dioxoperhydropyrido[1,2-c]pyrimidine skeleton are described. The most potent member of this series of eight diastereoisomers, (4aS,5R)-2-benzyl-5-[N-[(tert-butoxycarbonyl)-L-tryptophyl]-amino] - 1,3-dioxoperhydropyrido[1,2-c]pyrimidine, displays nanomolar CCK-A receptor affinity and higher than 8000-fold potency at the CCK-A than at the CCK-B receptor. As CCK-A antagonist, this compound inhibits the CCK-8-evoked amylase release from pancreatic acinar cells at a low concentration, similar to that of the typical antagonist Devazepide. Highly strict stereochemical requirements for CCK-A receptor binding and selectivity have been found. The L-Trp and the 4a,5-trans disposition of the bicyclic perhydropyrido[1,2-c]pyrimidine are essential for binding potency and selectivity.

Amylases↗
PubMed1997

YM022, a potent and selective gastrin/CCK-B receptor antagonist, inhibits peptone meal-induced gastric acid secretion in Heidenhain pouch dogs.

We examined the affinity of YM022, a potent and selective gastrin/CCK-B receptor antagonist, for canine gastrin/CCK-B and CCK-A receptors and the effects of YM022 on secretagogue- and peptone meal-induced acid secretion in the denervated, surgically separated (Heidenhain) canine gastric pouch model in comparison with those of famotidine, an H2-receptor antagonist, and atropine. YM022 inhibited the binding of [(125)I]CCK-8 and [(3)H]devazepide to canine gastrin/CCK-B and CCK-A receptors, with IC50 values of 0.73 and 136 nM, respectively. Intravenous YM022 dose-dependently inhibited pentagastrin- and peptone meal-induced acid secretion with ED50 values of 0.0261 and 0.0654 micromol/kg, respectively, without affecting histamine- or methacholine-induced acid secretion. Famotidine inhibited acid secretion induced by all stimulants, while atropine inhibited the acid secretion induced by every stimulant except histamine. These results indicated that YM022 is a highly potent and selective antagonist for the canine gastrin/CCK-B receptor and suppressed pentagastrin- and peptone meal-induced gastric acid secretion without affecting histamine- or methacholine-induced acid secretion in Heidenhain pouch dogs.

Animals↗
PubMed2002

Intestinal transit of fat depends on accelerating effect of cholecystokinin and slowing effect of an opioid pathway.

Fat has been described to both accelerate and slow intestinal transit. We hypothesized that the fat-induced jejunal brake depends on the combined accelerating effect of CCK and the slowing effect of an opioid pathway. Using a multifistulated model, intestinal transit was measured in four dogs, while 60 mM oleate was delivered into the proximal gut with either 0 or 6 mg naloxone, and 0.1 mg/kg devazepide (a peripheral CCK-A-receptor antagonist) administered intraluminally and intravenously, respectively. In a second study, intestinal transit was measured in seven dogs, while naloxone was delivered intraluminally at 0-, 3-, 6-, or 12-mg doses. Compared to the jejunal brake (marker recovery of 50.1 +/- 2.6%), intestinal transit was slowed by the CCK-A antagonist (36.4 +/- 8.3%; P < 0.05) and accelerated by naloxone (82.0 +/- 6.8%; P < 0.05). The accelerating effect of CCK occurred early in the transit response, while the dose-dependent effect (P < 0.05) of naloxone occurred later. We conclude that fat-induced jejunal brake depends on the early accelerating effect of CCK and the later slowing effect of a naloxone-sensitive opioid pathway.

Animals↗
PubMed1992

Influences of cholecystokinin octapeptide on phosphoinositide turnover in neonatal-rat brain cells.

Cholecystokinin octapeptide (CCK-8) has been shown to be coupled to phosphoinositide turnover in pancreatic acini as well as in a kind of neuroblastoma cell and a human embryonic cell line. Little is known, however, about its link with phosphatidylinositol breakdown in the brain. The brains (minus cerebella) from 1-2-day-old neonatal rats were enzymically dissociated into single cells. The intact cells were prelabelled by incubation with myo-[3H]inositol for 3 h, and were then stimulated with agonists in the presence of 10 mM-LiCl. Carbachol at 1 mM induced an increase in InsP3 labelling in brain cells (peak at 30 min, and then a gradual decrease), and a static accumulation of InsP with time, whereas the labelling of InsP2 remained essentially unchanged. A very similar time-response curve was obtained for 10 nM-CCK-8 in stimulating phosphoinositide turnover. The dose-response curve for incubated brain cells revealed that the formation of InsP3 increased when the concentration of CCK-8 was increased from 0.1 to 10 nM. A further increase in CCK-8 concentration to 100-1000 nM resulted in a gradual decrease in InsP3 formation. InsP and InsP2 levels stayed relatively stable. The production of InsP3 stimulated by 10 nM-CCK-8 was dose-dependently suppressed by the CCK-A antagonist Devazepide in the concentration range 1-10 nM; the effect declined when the concentration was further increased to 100-1000 nM. In contrast, the CCK-B antagonist L365,260 showed a sustained suppression of InsP3 production at concentrations above 0.1 nM, i.e. in the range 1-1000 nM. The results provide evidence that CCK-8 stimulates the turnover of phosphoinositide and increases InsP3 labelling in dissociated neonatal-rat brain cells, in which both CCK-A and CCK-B receptors seem to be involved.

Animals↗
PubMed1993

Feeding behaviour in chickens given diets containing medium chain triglyceride.

1. The effect of dietary medium chain triglyceride (MCT) on short-term food intake was compared with the effect of long chain triglyceride (LCT) in chickens. Maize oil was used as the LCT while glyceryl tricaprylate (C 8) and glyceryl tricaprate (C 10) were used as MCT. Cumulative food intake was determined during the 6 h after the start of feeding. 2. Chicks were given diets containing 200 g C 8/kg diet, 200 g C 10/kg diet or 200 g LCT/kg diet in experiment 1. As early as 30 min after feeding, cumulative food intake in both MCT-supplemented diets decreased significantly compared with the diet containing LCT. 3. To determine if endogenous cholecystokinin (CCK) was responsible for the decrease in food intake caused by MCT, birds were injected with the CCK-A receptor antagonist devazepide (DVZ, 1 mg/kg BW) before diet presentation. DVZ had no effect on food intake with either LCT- or MCT-supplemented diets. 4. In experiment 3, chicks were given a choice between either diets containing LCT and C 8, LCT and C 10, or C 8 and C 10 to confirm whether or not the palatability of the diets was influenced by the dietary fat sources. There was no difference in food intake between C 8 and C 10-supplemented diets. However, chicks preferred the LCT-supplemented diet compared with either of the diets containing MCT.

Animal Feed↗
PubMed2002

Involvement of cholecystokinin receptor in the inhibition of gastrointestinal motility by estradiol in ovariectomized rats.

BACKGROUND: The effects of estradiol benzoate (EB) on gastric emptying, gastrointestinal transit and plasma levels of cholecystokinin (CCK) were studied in ovariectomized rats. METHODS: Gastrointestinal motility was assessed in rats 15 min after intragastric instillation of a test meal containing charcoal and Na2 51CrO4. Gastric emptying was determined by measuring the amount of radiolabeled chromium contained in the small intestine as a percentage of the initial amount received. Gastrointestinal transit was evaluated by calculating the geometric center of distribution of the radiolabeled marker. Blood samples were collected for E2 and CCK radioimmunoassay. RESULTS: After treatment of EB (4-25 microg/kg), gastric emptying and gastrointestinal transit were inhibited, whereas plasma concentrations of E2 and CCK were increased in a dose-dependent manner. The selective CCK(A) receptor antagonists, devazepide and lorglumide, effectively attenuated the EB-induced inhibition of gastric emptying and gastrointestinal transit. L-365,260, a selective CCK(B) receptor antagonist, did not alter the EB-induced inhibition of gastric emptying and gastrointestinal transit. CONCLUSIONS: The results suggest that EB inhibits gastric emptying and gastrointestinal transit in ovariectomized rats via a mechanism involving CCK stimulation and CCK(A) receptor activation.

Animals↗
PubMed1999

The effect of bombesin, cholecystokinin, gastrin, and their antagonists on proliferation of pancreatic cancer cell lines.

BACKGROUND: The role of cholecystokinin (CCK) and gastrin in the development and growth of pancreatic cancer cells is controversial. The aim of this study was to evaluate the role of CCK-8S, gastrin-17, bombesin, and their antagonists on cell lines from patients with pancreatic cancer. METHODS: Cell lines were established from pancreatic cancers operated on at our department. The cells were grown in 10% fetal calf serum (FCS). The effects of CCK-8S, gastrin-17, bombesin, and their antagonists in different concentrations and for different time intervals were studied. The cell number was evaluated with the XTT method. RESULTS: The cell line LN 36 responded with increased cell number to stimulation by gastrin-17 and decreased cell number to inhibition by the CCK-B receptor antagonist L-365,260. In contrast, LPC 1 responded with increased cell number to CCK-8S and decreased cell number to the CCK-A receptor antagonist devazepide. LPC 2, 6, and 7 were stimulated by CCK-8S, gastrin-17, and their antagonists. LPC 3 showed decreased cell number after inhibition by the antagonists, and LPC 5 and 10 showed increased cell number after stimulation by CCK-8S and gastrin-17. LPC 4 was stimulated by CCK-8S, and LPC 8 was stimulated by all substances except gastrin-17. Intermittent administration of the substances to LN 36 led to a greater effect on the cell number than administration every day, which was not the case with LPC 1 and LPC 3. Bombesin led to an increased growth in LPC 5 but not in LPC 3. CONCLUSION: CCK-8S and gastrin-17 led to an increased cell number in some cell lines. A blockade of the CCK-A and CCK-B receptors by their antagonists led to an increased, an unaffected, or a decreased cell number of the cell lines. The effect of bombesin on different cell lines also varied. This shows a great heterogenicity among pancreatic cancer cells from different patients.

Benzodiazepinones↗
PubMed1997

Effects of high-fat diet and cholecystokinin receptor blockade on promotion of pancreatic ductal cell tumors in the hamster.

The mechanism by which high-fat diets potentiate pancreatic cancer is not known, but pancreaticotrophic hormones such as cholecystokinin (CCK) may be involved. The effect of CCK receptor blockade on carcinogenesis during the entire promotion period was investigated in Syrian Golden hamsters fed a high- or low-fat diet and treated with N-nitrosobis(2-oxopropyl)amine (3 x 10 mg/kg at weekly intervals). One-half of the hamsters fed a high-fat diet received the CCK-A receptor antagonist devazepide (25 nmol/kg/hr) for the duration of the experiment. At 39 weeks the incidence of pancreatic malignancies was significantly higher in hamsters fed the high-fat diet than in those fed the low-fat diet (p < 0.05). Tumor incidence was not changed by CCK receptor blockade. Potentiation of pancreatic cancer by a high-fat diet in hamsters does not appear to be influenced by endogenous CCK during the tumor promotion period.

Animals↗
PubMed2002

Dietary peptides induce satiety via cholecystokinin-A and peripheral opioid receptors in rats.

We hypothesized that the digestion of proteins gives rise to peptides that initiate several satiety signals from the gut, and that the signals arising will be dependent on the protein source. The role of peripheral opioid and cholecystokinin (CCK)-A receptors was investigated. Casein, soy protein, and casein and soy hydrolysates were administered to rats by gavage (0.5 g protein/4 mL water). Food intake was measured over 2 h. The opioid receptor antagonist, naloxone methiodide (1.0 mg/kg) given intraperitoneally (i.p.), increased food intake when given at the same time as the hydrolysate preloads, 25 min after the casein preloads and 55 min after the soy protein preloads. The CCK-A receptor antagonist, devazepide (which reverses protein-induced food intake suppression), when given at 0.25 mg/kg, i.p., 60 min before preloads of each of three soy hydrolysates, also blocked suppression of food intake, but the strength and duration of the interaction depended on the preparation. When the two receptor antagonists were both administered with soy or casein preloads, their effects were additive. We conclude that peptides arising from digestion contribute to satiety by independent activation of both opioid and CCK-A receptors.

Animals↗
PubMed2003

Soybean beta-conglycinin peptone suppresses food intake and gastric emptying by increasing plasma cholecystokinin levels in rats.

Cholecystokinin (CCK) is an important physiologic mediator that regulates satiety and gastric emptying. We demonstrated previously that soybean peptone acts directly on rat small intestinal mucosal cells to stimulate CCK release. In the present study, we examined the effects of beta-conglycinin, a major component of soy protein, and its peptone on food intake and gastric emptying after an intraduodenal infusion of beta-conglycinin peptone in relation to CCK release and interaction with the mucosal cell membrane. Intraduodenal infusion of beta-conglycinin peptone inhibited food intake in a dose-dependent manner, but that of whole soy peptone or camostat did not. The suppression of food intake by beta-conglycinin peptone was abolished by an intravenous injection of devazepide, a selective peripheral CCK receptor antagonist. The beta-conglycinin peptone infusion strongly suppressed gastric emptying with marked increases in portal CCK levels. We also observed that the beta-conglycinin peptone dose dependently and more potently stimulated CCK release from isolated dispersed mucosal cells of the rat jejunum than did beta-conglycinin itself. This stimulation corresponded to the binding activity of the peptide or protein to solubilized components of the rat jejunum membrane as evaluated by surface plasmon biosensor. These results indicate that beta-conglycinin peptone suppresses food intake, and this effect may be due to beta-conglycinin peptone in the lumen stimulating endogenous CCK release with direct acceptance to the intestinal cells.

Animals↗
PubMed2003

The addition of soybean phosphatidylcholine to triglyceride increases suppressive effects on food intake and gastric emptying in rats.

The physiologic roles of dietary lecithin have not yet been clearly defined. We examined the effects of soybean lecithin on gastric emptying (Experiments 1 and 2) and food intake (Experiment 3) in rats. Male Wistar rats were fed 2 g of a 20 g lipid/100 g diet containing various levels of lecithin after 24 h of food deprivation; gastric contents were collected 3 h after feeding (Experiment 1). In Experiment 2, the effects of lecithin and a CCK-A receptor antagonist on gastric emptying were examined using a modified phenol red recovery technique. In Experiment 3, their effects on food intake were examined after an intraduodenal infusion of an oil emulsion containing 50 mg soybean oil (SO) or SO partially replaced by lecithin (14-50%). Gastric emptying rates of the lipid and protein in the test diet (Experiment 1) or of phenol red (Experiment 2) were lower in the groups administered lecithin. Food intake for 60 min was lower in rats infused with the oil emulsion containing lecithin (25, 50%) than in rats not administered lecithin. The suppressive effects of lecithin on gastric emptying and food intake were largely reduced by devazepide. These results demonstrate that oil containing lecithin inhibits gastric emptying and food intake, and the effects are associated in part with CCK release.

Animal Feed↗
PubMed1995

Attenuation of gastrin-induced gastric acid secretion by antisense oligonucleotide to the CCKB/gastrin receptor.

The effects of treatment with CCK receptor antagonists or administration of an antisense oligonucleotide to the gastrin receptor, on gastrin-I and cholecystokinin-8-induced acid secretion in mouse stomach were evaluated. Administration of gastrin-I (1 microM) or cholecystokinin-8 (30 nM) stimulated acid output at the rates of 2.6 +/- 0.27 and 1.0 +/- 0.21 microEq h-1, respectively. Gastrin-I-induced acid output was significantly blocked by pretreatment of stomachs with 3R[+]-N-[2,3-dihydro-1-methyl-2-oxo-5- phenyl-1H-1,4-benzodiazepin-3-yl]-N[3-methylphenyl[urea (L-365,260; 1 microM), but not by devazepide (L-364,718; 1 microM). Cholecystokinin-8-induced acid output, on the other hand, was sensitive to both L-365,260 (100 nM) and L-364,718 (100 nM). Administration of antisense, but not mismatch, oligonucleotide significantly reduced gastrin-induced acid output, while antisense oligonucleotide treatment had no effect on cholecystokinin-8-induced acid output. These results of antagonist and antisense oligonucleotide studies suggest that gastrin-I and cholecystokinin-8 may involve different receptor subtypes in stimulating gastric acid secretion in mice, and that antisense oligonucleotide administration may serve an useful tool in characterizing CCK/gastrin receptor subtypes.

Animals↗
PubMed1996

Evidence for cholecystokininA receptors in bovine adrenal chromaffin cells.

We have studied a possible role of cholecystokinin (CCK) in regulating adrenal medullary function. Caerulein (10(-10)-10(-7) M), a CCK receptor agonist, increased formation of inositol phosphates in primary cultured bovine adrenal medullary (BAM) chromaffin cells in a concentration-dependent manner. The effect of caerulein was antagonized by devazepide, a selective CCKA-receptor antagonist, but not by L-365.260, a selective CCKB-receptor antagonist. These results suggest that BAM cells possess functional CCK receptors of the CCKA-subtype. Stimulation of these receptors with caerulein activates a signal transduction pathway via phospholipase C. CCK may regulate catecholamine release in BAM cells.

Adrenal Medulla↗
PubMed1995

The role of CCK and its analogues in the organogenesis of the fetal rat pancreas.

The gastrointestinal peptide cholecystokinin (CCK) has been shown to stimulate pancreatic growth in the adolescent and adult rat. However, little is known about the role of gastrointestinal hormones in the regulation of organ formation during fetal development. We therefore examined the effects of the CCK receptor antagonist devazepide (25 micrograms/h) and an antigastrin/CCK monoclonal immunoglobulin G on the maternal and fetal rat pancreas. These substances were infused subcutaneously with minipumps in female rats during the entire period of gestation. At the end of gestation, the rats were killed and the pancreata of the dams and their litter were examined for DNA and protein. In the dams, the receptor antagonist and the antibody against CCK/gastrin had no effect. In the newborns, the CCK receptor antagonist led to a significant reduction of the protein and DNA concentration [protein in controls, 105.0 +/- 3.75 micrograms/mg pancreatic tissue; in the antagonist group, 91.9 +/- 4.2 micrograms/mg pancreatic tissue (p < 0.05); DNA in controls, 1.28 +/- 0.19 micrograms/mg pancreatic tissue; in the antagonist group, 0.48 +/- 0.06 micrograms/mg pancreatic tissue (p < 0.05) (mean +/- SEM)]. Immune neutralization of CCK/gastrin in the maternal-fetal circulation induced a reduction of the protein concentration in the fetal pancreas (85.3 +/- 3.06 micrograms/mg pancreatic tissue; p < 0.01) but had no effect on fetal pancreatic DNA. Additional experiments indicated effective concentrations of the CCK receptor antagonist in fetal pancreatic tissue and free binding sites of the circulating antibody. In conclusion, the study provides evidence that CCK and its analogues are involved in fetal pancreatic organogenesis.

Animals↗
PubMed1997

Involvement of a CCK-dependent capsaicin-sensitive afferent pathway in the inhibitory effect of pinaverium bromide on the colonic motor response to eating in rats.

The effects of pinaverium bromide on the stimulation of colonic motility induced by meal and cholecystokinin (CCK) were investigated in rats chronically fitted with intraparietal electrodes on the proximal colon and previously treated or not by capsaicin. Pinaverium bromide inhibited in a dose-related manner (2-50 mg/kg, per os) the increase in colonic spike burst frequency induced by a 3 g meal or CCK-8 (2 micrograms/kg, i.v.). The CCK-A and CCK-B antagonists, devazepide and L 365260 (100 micrograms/kg, i.p.), respectively, inhibited the postprandial colonic motor response while only L 365260 reduced the CCK-induced stimulation. The effects of pinaverium bromide and CCK antagonists were not observed in capsaicin-treated animals. Moreover, CCK-8 (2 micrograms/kg, i.v.) did not stimulate colonic motility after capsaicin treatment. The inhibition of postprandial colonic motility by pinaverium bromide, given orally at therapeutic doses, involves a CCK-dependent pathway which requires the integrity of capsaicin-sensitive afferents.

Action Potentials↗
PubMed1994

Reversal of CRF- and dopamine-induced stimulation of colonic motility by CCK and igmesine (JO 1784) in the rat.

1. The role of dopamine in the genesis of corticotropin releasing factor (CRF)- and emotional stress (ES)-induced stimulation of colonic motility, as well as the mechanism of antagonistic action of cholecystokinin octapeptide (CCK-8s) and igmesine (alpha sigma receptor ligand, formerly JO 1784) on dopamine-induced colonic hypermotility, have been investigated in the rat. 2. ES and i.c.v. injection of CRF (0.5 microgram kg-1) increased the frequency of colonic spike bursts by 63% and 114%, respectively. Prior i.c.v. administration of (+)-SCH 23390 (a D1 receptor antagonist, 10 micrograms kg-1) significantly (P < 0.05) reduced the CRF- and ES-induced increase in colonic spike burst; whereas, sulpiride (a D2 receptor antagonist, 10 micrograms kg-1) blocked the CRF-induced stimulation of colonic spike bursts but had no effect on the colonic response to stress. 3. I.c.v. injection of dopamine (100 micrograms kg-1), increased colonic spike burst frequency by 54%. (+)-SKF 38393 (5 micrograms kg-1), a selective D1 receptor agonist, and quinpirole (5 micrograms kg-1), a selective D2 receptor agonist, increased colonic spike burst frequency by 71% and 70% respectively. CCK-8s (0.1 microgram kg-1) and igmesine (0.1 microgram kg-1) injected i.c.v. completely prevented the stimulatory effects of dopamine, (+)-SKF 38393 and quinpirole. 4. Previous i.c.v. injection of devazepide, a CCKA receptor antagonist, (10 micrograms kg-1) antagonized the inhibitory effects of both CCK-8s and igmesine injected i.c.v. on dopamine-induced colonic hyperkinesia. 5. These results show that CRF stimulates colonic motility through activation of central dopaminergic mechanisms in response to stress; furthermore, CCK-8s inhibits dopamine-induced colonic hyperkinesia through a mechanism involving D1 and D2 receptors. The sigma receptor ligand igmesine, blocks the CRF and ES-induced colonic hyperactivity via an interaction with central CCK mechanisms.

Action Potentials↗