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At least 19 recordsLinked to original sources
PubMed1993

Development of new lipophilic derivatives of tetragastrin: physicochemical characteristics and intestinal absorption of acyl-tetragastrin derivatives in rats.

In order to improve the intestinal absorption of tetragastrin (TG), we synthesized lipophilic derivatives of TG by acylation of its N-terminal amino group with acetic acid, caproic acid, and lauric acid. The purified TG derivatives, acetyl-tetragastrin (Ac-TG), caproyl-tetragastrin (Cap-TG), and lauroyl-tetragastrin (Lau-TG), were confirmed to be more lipophilic than the parent TG by high-performance liquid chromatography (HPLC). The pharmacological activities and the intestinal absorption of TG and its derivatives were examined by measuring gastric acid secretion. Stimulation of gastric acid secretion by these derivatives after intravenous administration was stronger than with native TG. When the acetyl- and caproyl-derivatives were administered into the large intestinal loops, a marked increase in gastric acid secretion was observed in comparison with TG, while no significant effect occurred following administration of the TG derivatives into the small intestines. These results indicated that chemical modification of TG with fatty acids improves the absorption of TG from the large intestines.

Acetates↗
PubMed1989

Effect of 6-hydroxydopamine on gastric carcinogenesis and tetragastrin inhibition of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of 6-hydroxydopamine (6-OHDA) on gastric carcinogenesis, on inhibition by tetragastrin of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine, and on the tissue catecholamine concentrations of the gastric wall and the labeling index of the gastric mucosa were investigated in inbred Wistar rats. Rats received s.c. injections of tetragastrin (1 mg/kg of body weight every other day) in depot form, i.p. injections of 6-OHDA (42 mg/kg twice within 24 h and 105 mg/kg every 2 wk), or injections of both compounds after 25 wk of p.o. treatment with N-methyl-N'-nitro-N-nitrosoguanidine (100 micrograms/ml). At Wk 52, prolonged administration of tetragastrin or 6-OHDA had significantly reduced the incidence and the number of adenocarcinomas. Combined administration of tetragastrin and 6-OHDA significantly enhanced the inhibitory effects of tetragastrin or 6-OHDA on gastric carcinogenesis. Administration of 6-OHDA but not tetragastrin, caused a significant decrease in norepinephrine concentrations in the antral portion of the gastric wall. Rats treated with tetragastrin or 6-OHDA had a significantly lower labelling index of the antral mucosa, and this index was significantly decreased by combined administration of tetragastrin and 6-OHDA, as compared with labeling indices observed after treatment with tetragastrin or 6-OHDA alone. These findings indicate that 6-OHDA exerts a protective effect against gastric carcinogenesis and enhances the inhibitory effect of tetragastrin on gastric carcinogenesis. This effect of 6-OHDA may be related to its ability to inhibit cell proliferation of the antral mucosa.

Animals↗
PubMed1990

Effect of ornithine decarboxylase inhibitor on tetragastrin treatment of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of combined administration of tetragastrin and the ornithine decarboxylase inhibitor 1,3-diaminopropane (DAP) on the incidence and number of gastric cancers induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and the BUdR labelling indices of the fundic and antral mucosae, were investigated in inbred Wistar rats. Rats were given drinking water containing 2.5 g/l of DAP ad libitum and received alternate-day injections of 1 mg/kg body weight of tetragastrin in depot form after 25 weeks of oral treatment with MNNG. At week 52, prolonged administration of tetragastrin alone resulted in a significant reduction in the incidence and number of gastric cancers and a significant increase or decrease in the labelling indices of the fundic and antral mucosae, respectively. Concomitant administration of tetragastrin and DAP had no effect on the inhibition by tetragastrin of gastric carcinogenesis. With this treatment, the labelling index was significantly reduced in the fundic mucosa but not in the antral mucosa. These results suggest that ODC inhibitor does not attenuate tetragastrin inhibition of gastric carcinogenesis, and that anti-trophic action of tetragastrin on antral mucosa may be related to tetragastrin inhibition of gastric carcinogenesis.

Animals↗
PubMed1988

Inhibition by tetragastrin of experimental carcinogenesis in rat colon: effect of wheat bran consumption.

The effect of dietary wheat bran consumption on the anticarcinogenic action of tetragastrin upon colon carcinogenesis induced by azoxymethane was investigated in 122 inbred Wistar rats. Rats were given a control fiber-free diet or the same basal diet plus 20% wheat bran. From week 5, they were given 250 micrograms per kg body weight of tetragastrin in depot form every other day until the end of the experiment at week 45. Prolonged administration of tetragastrin resulted in a significant reduction of the incidence and number of colonic tumors per rat in the group given the fiber-free diet. The adenocarcinomas that did develop in this group had high mucin-producing activity, unlike the cancers produced in controls without tetragastrin. However, administration of tetragastrin had little or no influence on the incidence, number or histology of colonic tumors in the group given basal diet plus wheat bran. Dietary supplementation with wheat bran alone had little or no effect on the development or histology of colonic tumors. Before and during the administration of carcinogens, addition of fiber to the diet resulted in a significant fall in the colonic pH and a significant increase in the crypt column length, but administration of tetragastrin did not have an additive effect on the crypt column length in rats fed diet supplemented with fiber.

Adenocarcinoma↗
PubMed1992

Effects of tetragastrin on mucus glycoprotein in rat gastric mucosal protection.

The effects of tetragastrin on mucus glycoprotein (mucin) metabolism and mucosal protection in rat gastric mucosa were investigated. Rats were administered with various doses of tetragastrin (12, 120, or 400 micrograms/kg body weight; s.c.), followed by 50% ethanol-induced gastric injury. Tetragastrin caused a significant increase in mucin content in the corpus mucosa and prevented 50% ethanol-induced gastric mucosal damage in a dose-dependent manner. For assessment of the effects of tetragastrin on the metabolism of gastric mucin in detail, changes in mucin distribution in the three different layers of rat gastric mucosa were examined one hour after single administration of tetragastrin. A significant increase in the mucin content was noted in the mucus gel and surface mucosal layer. Mucin content in the deep mucosa corresponding mainly to the mucus neck cell mucin underwent virtually no change by this treatment. An increase in mucin in the mucus gel and surface mucosa would thus appear due to the administration of tetragastrin and may possibly be related to the protective action of the gastric mucosa against injury. The data demonstrate a possibility that gastrin may have potential for enhancing gastric mucosal protection associated with mucus secretion and/or mucus synthesis on the surface mucosa of rat gastric mucosa.

Animals↗
PubMed1988

Effect of cimetidine on inhibition by tetragastrin of carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of combined administration of cimetidine and tetragastrin on gastric acid secretion, the labeling index of the gastric mucosa, and the incidence of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in inbred Wistar rats. Prolonged administration of tetragastrin in depot form after treatment with N-methyl-N'-nitro-N-nitrosoguanidine resulted in a significant increase in gastric acid secretion, a significant decrease in the labeling index of the antral mucosa, and a significant decrease in the incidence of adenocarcinomas of the glandular stomach. Administration of cimetidine at 20 mg, but not 10 mg, per kg body weight with tetragastrin significantly reduced the gastric acid secretion induced by tetragastrin alone but did not influence the labeling index of the antral mucosa or the inhibitory effect of tetragastrin on gastric carcinogenesis. These findings indicate that gastric acid secretion has no influence on the development of gastric adenocarcinomas and that the inhibitory effect of tetragastrin on gastric carcinogenesis may be related to its effect in decreasing proliferation of cells in the antral mucosa.

Adenocarcinoma↗
PubMed1987

Enhancement by propranolol of the inhibitory effect of tetragastrin on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of combined administration of propranolol and tetragastrin on gastric acid secretion and the incidence and histological types of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in inbred Wistar rats. Prolonged administration of tetragastrin, 1 but not 0.2 mg/kg body weight in depot form after treatment with N-methyl-N'-nitro-N-nitrosoguanidine significantly reduced the incidence of adenocarcinoma of the glandular stomach. The adenocarcinomas that did develop in rats treated with the higher dose of tetragastrin had high mucin-producing activity and showed little or no typical glandular structure. A combination of propranolol (2 mg/kg) and tetragastrin (1 mg/kg) did not influence the inhibitory effect of gastrin on gastric carcinogenesis. However, concomitant administration of propranolol (2 mg/kg) and tetragastrin (0.2 mg/kg) caused a significant increase in gastric acid secretion and a reduction in the incidence of gastric carcinomas. With this treatment, the incidence of adenocarcinoma was similar to that of treatment with tetragastrin (1 mg/kg). Histological examinations showed that like the cancers in control rats, the adenocarcinomas induced in these rats were all highly differentiated.

Adenocarcinoma↗
PubMed1988

Inhibitory effect of prolonged administration of tetragastrin on experimentally induced intestinal metaplasia in Wistar rats.

The effect of tetragastrin on the induction of intestinal metaplasia by intragastric administration of 5% NaOH solution was investigated in Wistar rats. The prolonged administration of tetragastrin in depot form from 1 week after NaOH treatment resulted in a significant increase in basal gastric acid secretion and a significant reduction in the incidence and number of intestinal metaplasia in experiment week 35. A histologic examination showed goblet cell metaplasia and intestinal metaplasia without Paneth cells in rats treated only with olive oil. Only goblet cell metaplasia was found in rats treated with tetragastrin. These results show that the prolonged administration of tetragastrin to rats after NaOH treatment increases gastric acid secretion and suppresses the induction of intestinal metaplasia.

Animals↗
PubMed1986

Release of endogenous prostaglandins by mild hyperosmotic saline inhibits tetragastrin-stimulated gastric acid secretion in rats.

Filling of the gastric lumen of rats with 1.0 M NaCl solution (5 ml) for 10 min under urethane anesthesia caused an increase in the gastric fluid concentrations of prostaglandin (PG) E2, 13,14-dihydro-15-keto-PGE2 and 6-keto-PGF1 alpha as determined by radioimmunoassay. PGE2 was the major PG generated. The levels of PGE2 in the gastric fluid were increased dose-dependently after filling the lumen with 0.3, 0.5, 0.7 or 1.0 M NaCl solutions. The pH of the gastric fluid increased similarly after 0.5 to 1.0 M NaCl solutions. Indomethacin (10 mg/kg, i.p.) suppressed the PGE2 increase caused by 1.0 M NaCl solution, but did not prevent the increase of the pH of the gastric fluid induced by intragastric 1.0 M NaCl. Infusion of tetragastrin (62.5 micrograms/kg/hr, i.v., for 10 min) caused a marked increase of acid secretion without modifying intragastric concentration of PGE2. The acid secretion due to tetragastrin was completely inhibited after intragastric administration of 1.0 M NaCl solution, while indomethacin restored the tetragastrin-induced acid secretion, with prevention of a rise of intragastric PGE2 levels. These observations suggest that 1.0 M NaCl solutions suppress basal intragastric acid through a mechanism which is independent of prostaglandins. In contrast, the suppression of tetragastrin-induced acid secretion by intragastric 1.0 M NaCl solution appears to be mediated through a release of prostaglandins.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Inhibitory effects of tetragastrin and histamine on carcinogenesis in the small intestines of W rats by N-methyl-N'-nitro-N-nitrosoguanidine.

The effects of tetragastrin and histamine on the incidence and histology of tumors induced in the small intestine by N-methyl-N'-nitro-N-nitrosoguanidine [(MNNG) CAS: 70-25-7] were investigated in male W rats. Animals were given MNNG at 150 micrograms/ml in their drinking water for 25 weeks and then 300 micrograms tetragastrin or 4 mg histamine dihydrochloride sc per day in depot form. Administration of tetragastrin or histamine after MNNG treatment resulted in a significant increase in gastric acid secretion and a significant reduction in the incidence of tumors in the duodenum; however, only histamine decreased the incidence of tumors in the jejunum. Histologically, the tumors induced in the small intestine were mostly adenocarcinomas, and their histologic type was not affected by either tetragastrin or histamine.

Adenocarcinoma↗
PubMed1986

Effect of tetragastrin on the colonic mucosa of rats during intrarectal administration of N-methyl-N'-nitro-N-nitrosoguanidine.

The effects of the C-terminal tetrapeptide of gastrin, tetragastrin, on the colonic mucosa on Days 15 and 25 during intrarectal administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and its effects on the incidences of colonic tumors in experimental Wk 20 and 35 were investigated in Wistar rats. Administration of tetragastrin in depot form during instillation of MNNG resulted in significant decreases in the incidences of mucosal erosions, ulcerations, and atypical regenerative glandular hyperplasias in the colonic mucosa, most of these lesions being greater in the distal half of the colon. Administration of tetragastrin also significantly decreased the incidences and/or numbers of colonic tumors in Wk 20 and 35. The distribution of colonic tumors induced in Wk 20 and 35 corresponded well to those of erosions, ulcerations, and atypical regenerative glandular hyperplasias induced during the administration of MNNG. These findings suggest that the effect of tetragastrin in decreasing the incidences of erosions, ulcerations, and atypical regenerative glandular hyperplasias in the colonic mucosa during instillation of MNNG is related to its effect in reducing the development of colonic tumors.

Animals↗
PubMed1981

[Tetragastrin activation of rat gastric mucosa adenyl cyclase in vitro].

The effect of tetragastrin and histamine on the adenylate cyclase activity of the rat gastric mucosa was examined in vitro. Tetragastrin and histamine were demonstrated to stimulate the activity of the enzyme in question. The antagonist of histamine H2-receptors, cimetidine inhibits the stimulatory effect of histamine in vitro and activates tetragastrin stimulation of the adenylate cyclase activity. It is suggested that tetragastrin and histamine activate adenylate cyclase of the rat gastric mucosa via different receptors.

Adenylyl Cyclases↗
PubMed1990

Effect of tetragastrin on azaserine-induced carcinogenesis in rat pancreas.

The effect of tetragastrin on pancreatic tumors induced by azaserine was investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight of azaserine and 1 mg/kg body weight of tetragastrin as a suspension in olive oil every other day. Carcinogen-induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histological analysis showed that prolonged administration of tetragastrin had little or no influence on the number and size of the carcinogen-induced pancreatic lesions, although it caused significantly increased cell proliferation, indicated by a greater labelling index of the pancreatic acinar cells.

Adenosine Triphosphatases↗
PubMed1982

Effect of a test meal, duodenal acidification, and tetragastrin on the plasma concentration of beta-endorphin-like immunoreactivity in man.

The effects of various test materials on plasma beta-endorphin-like immunoreactivity (beta-EpLI) were investigated in man using a specific radioimmunoassay developed by the authors. Plasma beta-EpLI was determined after extraction by the acid/acetone method (recovery 73 +/- 5%). The intraassay and interassay coefficients of variation were 5.0% and 7.6%, respectively. The plasma concentrations of human beta-EpLI in normal subjects were 11.6 +/- 4.0 pmol/l for men (n = 23) and 10.7 +/- 4.8 pmol/l for women (n = 27). Ingestion of a test meal (150 g of Campbell's condensed meat soup) resulted in a biphasic rise in plasma beta-EpLI from the basal level of 4.4 +/- 1.0 pmol/l to 29.2 +/- 1.9 pmol/l after 5 min and 24.8 +/- 6.7 pmol/l after 90 min. Intraduodenal infusion of 115 ml of 0.1 M HCl over 10 min increased the plasma beta-EpLI level from 8.7 +/- 0.5 pmol/l to 15.5 +/- 0.4 pmol/l at 10 min after the start of infusion, but the level rapidly returned to the initial value after the end of the infusion. Intramuscular injection of 4 micrograms/kg body weight of tetragastrin markedly stimulated gastric acid output and beta-EpLI release, but pretreatment with 10 mg of histamine H2 receptor antagonist inhibited the gastric acid output and plasma beta-EpLI release induced by tetragastrin. These results indicate that beta-EpLI release is stimulated by ingestion of meat soup, duodenal acidification and tetragastrin administration. It is suggested that gastric acid participates, at least in part, in postprandial release of beta-EpLI, probably from the gastrointestinal tract.

Adult↗
PubMed1989

Enhancement by tetragastrin of experimental induction of gastric epithelium in the duodenum.

The effects of tetragastrin and truncal vagotomy on the incidence of gastric type epithelium in the duodenum by intraduodenal instillation of 5% NaOH solution were investigated in Wistar rats. Prolonged administration of 1 mg tetragastrin/kg body weight in depot form starting one week after NaOH treatment resulted in a significant increase in gastric acid secretion and the incidence and number of villi with gastric epithelium in the duodenum in experimental week 10. Villi with gastric epithelium were found in five (23%) of 22 rats in control group, whereas abnormal villi were found in 13 (59%) of 22 rats in the tetragastrin treated group (p less than 0.05). The average number of villi with gastric epithelium rose from 0.6 (0.4) per 100 villi in control rats to 2.4 (0.6) per 100 villi in tetragastrin treated rats (p less than 0.01). On histological examination, gastric type epithelium was most often found on stunted or flattened villi, and was always within the boundaries of the area of Brunner's glands. These mucosal changes reverted toward normal with time. In week 35, the incidence of gastric epithelium was significantly less than at week 10 (p less than 0.05). In contrast, no villi with gastric epithelium were found in vagotomised rats in week 10 (p less than 0.05). Vagotomy also caused a significant decrease in gastric acid secretion. These results show that exposure of the duodenal mucosa to high levels of gastric acid enhance the induction of gastric eithelium in the duodenum.

Animals↗
PubMed1984

'In vivo' amplification of biological activity of tetragastrin by amino acid hydroxamates.

Rat blood was shown to contain an aminopeptidase which rapidly hydrolyses short peptides containing an aromatic amino acid as N-terminal residue. Using tetragastrin (Trp-Met-Asp-PheNH2) as substrate, we showed that some amino acid hydroxamates inhibit rat aminopeptidase activity 'in vitro' in the following order: HTrpNHOH greater than HPheNHOH much greater than HAlaNHOH. The same hydroxamates markedly enhanced the biological activity of tetragastrin 'in vivo'. The amplification of the secretory effect, correlated with the amount of the hydroxamate used, strongly suggests that these compounds can stabilize a number of active peptides in vivo by inhibiting their proteolytic degradation.

Amino Acids↗
PubMed1988

Increased parietal cell responsiveness to tetragastrin in patients with recurrent duodenal ulcer.

To clarify the contributive factors in the recurrence of duodenal ulcer, the present study was carried out on 65 male patients with active duodenal ulcers and 20 healthy male subjects. After having verified that the ulcer had healed, gastric acid secretory responses to graded doses of tetragastrin from 62.5 to 16,000 ng/kg/hr were investigated using a logarithmic transformation model. Several clinical features were also investigated. The patients were divided into three groups based on the later endoscopic follow-up study for two years. The early-recurrent group included 16 patients with recurrence occurring within three months. The late-recurrent group included 25 with recurrence occurring after three months. The nonrecurrent group included 24 patients without recurrences during the follow-up period. The 20 healthy male subjects were defined as a control group. The results were as follows: (1) Significant differences were not discerned either in basal and peak acid outputs between the three patients groups. (2) The ED50 value for tetragastrin was lower in the early-recurrent group than in the other three groups. (3) The early-recurrent group showed a higher percentage of smokers than the other patient groups. These results suggest that smoking and increased parietal cell responsiveness correlates strongly with duodenal ulcer recurrence.

Adult↗