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PubMed1992

Role of cholecystokinin in the inhibition of gastric acid secretion in dogs.

1. This study was designed to determine the involvement of cholecystokinin (CCK) in the gastric secretory responses to exogenous and endogenous secretagogues in conscious dogs with chronic gastric fistulae (GF), pancreatic fistulae (PF) and Heidenhain pouches (HP). 2. A meal of meat or intragastric application of peptone (300 mosM) increased secretion of HCl from the HP and pancreatic secretion of protein and plasma levels of gastrin, CCK and somatostatin. 3. The CCK receptor antagonist L-364,718 caused a further increase in the postprandial HCl secretion from the HP and in the plasma levels of gastrin and CCK but pancreatic output of protein and plasma concentration of somatostatin were significantly reduced. 4. Addition to intragastric peptone of 10% oleate or its acidification to pH 3.0 profoundly inhibited the HP secretion and gastrin release but significantly increased pancreatic secretion of protein and plasma levels of CCK and somatostatin. Administration of L-364,718 reversed the fall in the HP secretion and plasma gastrin while significantly attenuating pancreatic protein secretion and plasma somatostatin levels. 5. Intragastric administration of hyperosmolar (1200 mosM) peptone also inhibited HCl secretion from the HP but this was not affected by L-364,718. 6. Exogenous CCK and bombesin (but not gastrin) caused a small increase in HCl secretion from the HP and marked stimulation of pancreatic protein secretion accompanied by a significant rise in plasma levels of gastrin, CCK and somatostatin. Administration of L-364,718 resulted in a further increase in the HCl response of HP to bombesin and in plasma levels of gastrin and CCK but caused a reduction in plasma levels of somatostatin. 7. We conclude that CCK released by a meal of meat, intragastric peptone, oleate or acidified peptone and intravenous bombesin exerts tonic inhibitory influences on gastric acid secretion and that this effect is mediated, at least in part, by somatostatin.

Animals↗
PubMed1978

Organ culture studies of rat antrum: evidence for an antral inhibitor of gastrin release.

The regulation of gastrin release in rodent antral mucosal organ cultures was investigated. The tissue was well preserved morphologically and medium gastrin concentration increased steadily throughout a 24-h culture period. The effects of peptone and a bovine serum albumin digest on gastrin release were independently investigated. During the periods these agents were in contact with the tissue, medium gastrin concentration did not differ from those of control cultures. However, treatment cultures released a significantly greater amount of gastrin into the medium than did control cultures during the two posttreatment periods. Prolongation of the period of exposure to peptone did not alter this secretory pattern. The rise in medium gastrin concentration that followed the removal of peptone was directly related to the medium peptone concentration and was partially inhibited by readdition of peptone to cultured antral explants. These results suggest that substances which stimulate gastrin release in vivo may cause the accumulation of an antral inhibitor of gastrin release when exposed to rat antral mucosa in culture.

Animals↗
PubMed1984

Role of endogenous secretin in acid-induced inhibition of human gastric function.

The role of secretin in the inhibition of gastric acid secretion that occurs during acidification of the gastric lumen was studied in nine healthy men. Gastric acid secretion was stimulated by 500-ml meals of 8% peptone solution, and the pH of the stomach was maintained at 5.5, 2.5, or 2.0 by intragastric titration. The increase in plasma secretin was measured, after extraction, by a new secretin radioimmunoassay. After determining the intravenous dose of secretin required to reproduce plasma secretin concentrations achieved during pH 2.5 and 2.0 meals, similar doses were given during administration of a pH 5.5 peptone meal. The doses of secretin led to plasma secretin concentrations that averaged 3.4 pM, not different from the 3.2 and 3.9 pM concentrations achieved during acidified meals. However, exogenous secretin infusion failed to inhibit acid secretion or gastrin response to peptone, although significant inhibitions occurred in both during peptone meals given at pH 2.5 or 2.0. When secretin infusions were given at fivefold higher rates, plasma gastrin responses again failed to demonstrate significant inhibition. Gastric emptying was inhibited significantly by both acidified peptone meals but only slightly (P = 0.053) during exogenous infusion of physiologic secretin doses. The decrease in acid secretion could be explained by decreased gastrin release, but neither of these findings could be explained by circulating secretin concentrations. These results cast strong doubt on a physiological role of secretin in inhibition of acid secretion in man.

Adult↗
PubMed1990

Action of neurotensin on meal-stimulated gastric acid secretion in the dog.

In six to nine mongrel dogs the effect of graded doses of intravenous neurotensin (188, 375, 750, and 1500 pmol/kg h) on acid secretion basally or stimulated by distention (by isotonic glucose), peptone (0.5, 1, and 4 g%), and pentagastrin was studied. Neurotensin did not affect acid secretion basally, stimulated by distention, or the maximal peptone dose. However, when submaximal doses (0.5 and 1 g%) of peptone were instilled in the stomach, neurotensin stimulated the secretory response to intragastric peptone. This effect was observed in doses of intravenous neurotensin which mimicked circulating neurotensin concentrations after a standard test meal. Thus, neurotensin could be considered a physiologic stimulant of acid secretion when protein is present in the stomach. The mechanism for this action of neurotensin is unknown but could be partly explained by an enhanced release of gastrin. The potentiating effect of neurotensin on peptone-stimulated acid secretion could play a major role in gastric secretory function of the dog.

Animals↗
PubMed1992

Regulation of gastric acid secretion by gastrin in duodenal ulcer patients and healthy subjects.

To examine the role of gastrin as a major mediator of meal-stimulated acid secretion at low and high intragastric pH, gastric acid secretory responses after exogenous and endogenous stimulation were studied in relation to circulating plasma gastrin levels in 19 healthy control subjects and in 18 patients with inactive duodenal ulcer disease. Gastrin was given intravenously in stepwise fourfold-increasing doses from 3.1 to 800 pmol.kg-1.h-1 over consecutive 30-minute periods. Circulating plasma gastrin and acid secretion rates, measured by intragastric titration, were compared with the values obtained during endogenous stimulation by intragastric meals of 0.5, 1, 2, 4, and 8 g% peptone at either pH 5.5 or pH 2.5. The studies showed that circulating gastrin is a major regulator of acid secretion in the presence of peptone in both healthy controls and subjects with duodenal ulcers. Patients with duodenal ulcers had higher acid secretion rates in response to endogenous and exogenous stimulation. In duodenal ulcer subjects and healthy controls, acid secretion in response to higher doses (2-8 g%) of peptone was inhibited at low intragastric pH. This pH inhibition could be fully explained by diminished gastrin release. Patients in the DU group differed from the controls by diminished inhibition of acid secretion at intragastric pH 2.5 when low doses (1 g%) of peptone meals were used. In summary, gastrin is a major regulator of endogenously stimulated acid secretion at high and low intragastric pH in healthy subjects. DU patients differ from healthy controls by higher total acid secretion rates and diminished inhibition of acid secretion when low concentrations of peptone are present in the stomach.

Adult↗
PubMed1979

[Comparative tests of various liquid media for the preenrichment of salmonellae from milk powder (author's transl)].

In applying S. mendoza the following four liquid media were tested as to whether they can be used as enrichment broths for salmonellae in milk powder: phosphate buffered water, correspondingly buffered peptone broth, tetrathionate and selenite lactose broth. The yield of salmonellae in these tests is largely independent of the starting pH value of the prepared milk suspension which was varied between 5.8 and 8.2 (Fig. 1). In water the pH dropped within 24 hours (Fig. 2), in peptone and tetrathionate broth within 48 hours down to figures between 4.1 and 4.4 (Fig. 3 and 4), in selenite broth final figures of pH 5.7 were not attained before the lapse of 6 days (Fig. 5). The absolutely highest germ figures were observed in selenite broth. Quite in general the bacteria figure maximum was not attained until the 3rd--5th day, whereupon the germ figures dropped again. In peptone broth the introduced salmonellae were recovered in 73% of all cases after the lapse of 24 hours. Also in tetrathionate the success quota was about 73%, but part of it (8%) did not increase until a lapse of more than 72 hours incubation time, although the pH had already become strongly acid some days previously. In water the introduced salmonellae were traced only in 67%, in selenite broth even only in 61%. Also the time until the first detection increased a little in these media (Table 1). The period during which salmonellae were traceable was equally highest in peptone broth being 57% relative to the complete testing period (tetrathionate: 55%, water: 51%, selenite: 39% (Table 1). This permits the conclusion that peptone broth is the best preenrichment medium in which salmonellae may become traceable after a lapse of approx. 24 hours. Not considerably more unfavourable is the tetrathionate broth which so far had been considered as an exclusive selectivity medium. In this context it is, however, necessary to face the possibility that predamaged salmonellae do not begin to increase until the end of some days incubation and even at a strongly acid pH.

Animals↗
PubMed1998

Effects of YF476, a potent and selective gastrin/cholecystokinin-B receptor antagonist, on gastric acid secretion in beagle dogs with gastric fistula.

The antisecretory effects of the gastrin/cholecystokinin-B (CCK-B) receptor antagonist YF476 ((R)-1-[2,3-dihydro-2-oxo-1-pivaloylmethyl-5-(2'-pyridyl) 1H-1,4-benzodiazepin-3-yl]-3-(3-methylaminophenyl)-urea, CAS 155488-25-8) on secretagogue- and peptone-induced gastric acid secretion in beagle dogs with chronic gastric fistula were examined. Plasma gastrin concentrations were evaluated following introduction of peptone into the stomach. Intravenous administration of YF476 dose-dependently inhibited pentagastrin (1 microgram/kg/h)-induced gastric acid secretion, with an ED50 value of 0.0023 mumol/kg. In contrast, intravenous administration of YF476 (0.3 mumol/kg) did not affect histamine (15 micrograms/kg/ h)-induced gastric acid secretion. Oral administration of YF476, famotidine and omeprazole dose-dependently inhibited peptone (8%, 200 ml)-induced gastric acid secretion with ED50 values of 0.11, 0.76 and 4.28 mumol/kg, respectively. The antisecretory effect of YF476 was about 7 and 40 times more potent than that of famotidine and omeprazole, respectively. Plasma gastrin concentrations were increased by introduction of peptone. These results suggest that YF476 is an extremely potent and selective antisecretory drug and the endogenous gastrin plays an important role in peptone-induced gastric acid secretion in dogs.

Animals↗
PubMed2001

Biomass production and secretion of hydrolytic enzymes are influenced by the structural complexity of the nitrogen source in Fusarium oxysporum and Aspergillus nidulans.

The structural complexity of the nitrogen sources strongly affects biomass production and secretion of hydrolytic enzymes in filamentous fungi. Fusarium oxysporum and Aspergillus nidulans were grown in media containing glucose or starch, and supplemented with a nitrogen source varying from a single ammonium salt (ammonium sulfate) to free amino acids (casamino acids), peptides (peptone) and protein (gelatin). In glucose, when the initial pH was adjusted to 5.0, for both microorganisms, higher biomass production occurred upon supplementation with a nitrogen source in the peptide form (peptone and gelatin). With a close to neutrality pH, biomass accumulation was lower only in the presence of the ammonium salt. When grown in starch, biomass accumulation and secretion of hydrolytic enzymes (amylolytic and proteolytic) by Fusarium also depended on the nature of the nitrogen supplement and the pH. When the initial pH was adjusted to 5.0, higher growth and higher amylolytic activities were detected in the media supplemented with peptone, gelatin and casamino acids. However, at pH 7.0, higher biomass accumulation and higher amylolytic activities were observed upon supplementation with peptone or gelatin. Ammonium sulfate and casamino acids induced a lower production of biomass, and a different level of amylolytic enzyme secretion: high in ammonium sulfate and low in casamino acids. Secretion of proteolytic activity was always higher in the media supplemented with peptone and gelatin. Aspergillus, when grown in starch, was not as dependent as Fusarium on the nature of nitrogen source or the pH. The results described in this work indicate that the metabolism of fungi is regulated not only by pH, but also by the level of structural complexity of the nitrogen source in correlation to the carbon source.

Amylases↗
PubMed2004

Protein hydrolysates stimulate proglucagon gene transcription in intestinal endocrine cells via two elements related to cyclic AMP response element.

AIMS/HYPOTHESIS: Protein hydrolysates (peptones) increase not only glucagon-like peptide-1 (GLP-1) secretion but also transcription of the proglucagon ( PG) gene in the intestine. The critical physiological roles of gut-derived GLPs raised hope for their therapeutic use in several disorders, especially GLP-1 in diabetes. We aimed to investigate the molecular mechanisms involved in this nutrient- PG gene interaction. METHODS: Wild-type and mutated PG promoter fragments fused to the luciferase reporter gene were transfected into enteroendocrine STC-1 cells, which were then either treated or not with peptones. Co-transfection with expression vectors of dominant-negative forms of cAMP response element binding protein (CREB) and protein kinase A (PKA) proteins were performed, as well as electrophoresis mobility shift assays. RESULTS: Deletion analysis showed that the promoter region spanning between -350 and -292 bp was crucial for the transcriptional stimulation induced by peptones. Site-directed mutagenesis of the canonical cAMP response element (CRE(PG)) and of the adjacent putative CRE site (CRE-like1) led to a dramatic inhibition of the promoter responsiveness to peptones. Over expression of a dominant-negative mutant of CREB or of PKA produced a comparable and selective inhibitory effect on the activity of transfected promoter fragment containing the -350/-292 sequence. EMSA showed that CREB and fra2 transcription factors bound to CRE(PG) and CRE-like1 elements respectively, independently of peptone treatment. CONCLUSIONS/INTERPRETATION: Our report identified cis- and trans-regulatory elements implicated in the transcriptional control of PG gene by nutrients in enteroendocrine cells. It highlights the role of a previously unsuspected CRE-like1 element, and emphasises the importance of CRE-related sequences in the regulation of PG gene transcription in the intestine.

Animals↗
PubMed1995

Stability of 1-nitropyrene and 1,6-dinitropyrene in environmental water samples and soil suspensions.

This study examined the stability of mutagenic 1-nitropyrene (1-NP) and (1,6-dinitropyrene (1,6-diNP) in environmental water samples and various soil suspensions containing 0.1% peptone and in water samples containing no peptone. The water samples or the soil suspensions were mixed with NPs and incubated at 30 degrees C. The stability of NPs was expressed as mutagenic activity remaining in the test solutions. The mutagenicity decreased rapidly when 1-NP or 1,6-diNP was incubated in unautoclaved test solutions containing 0.1% peptone but not when incubated in autoclaved test solutions. The mutagenicity in the soil suspensions, especially in the sludge, decreased faster than in the water samples. This was due to the large number of colony-forming units (CFU) in the soil suspensions. In the water samples containing 0.1% peptone, the mutagenicity of NPs in the polluted Tamiya River water decreased faster than in the unpolluted Yoshino River water. The rate of decrease was dependent on the number of CFU in the water samples. A large number of CFU decreased the mutagenicity more rapidly than did a small number of CFU in samples. The disappearance of mutagenicity was dependent on the initial concentrations of NPs. The periods required for a 50% decrease in the mutagenicity of 1-NP at the low concentration (0.2 microgram/ml) was shorter than that at the high concentration (3 micrograms/ml). 1-Aminopyrene was detected in the 1-NP test solution after incubation when it was analyzed by high-pressure liquid chromatography. In the water samples containing no peptone, the mutagenicity of 1-NP (0.2 microgram/ml) decreased gradually during 30 days of incubation. After incubation for 1540 days, the remaining mutagenicity of 1-NP in the water samples was almost the same as that in autoclaved water samples. On the other hand, the mutagenicity of 1,6-diNP (10 ng/ml) decreased and the remaining mutagenicity, except in the Yoshino River water, was less than 20% after 30 days of incubation and was completely lost during the 1540-day incubation. However, the mutagenicity of 1,6-diNP in autoclaved water samples was very stable and almost all mutagenicity, except in sea water, remained after 1540 days of incubation at 30 degrees C. These results suggest that the microflora in the environment plays an important role in the primary degradation and decontamination of relatively low concentrations of NPs.

Biodegradation, Environmental↗
PubMed1997

Effect of diluent type on viability of yeasts enumerated from foods or pure culture.

The effects of seven diluent types on the viability of yeasts enumerated from foods and in pure culture were studied. The diluents were laboratory glass distilled water; saline water (0.85% NaCl), sodium phosphate buffer (0.1 M, pH 7.0), 0.1% peptone, 0.1% yeast extract, 0.1% peptone in 0.1 M sodium phosphate buffer, pH 7.0, and 0.1% malt extract. For all foods studied, dilution in 0.1% peptone gave the highest counts, with saline and phosphate buffer diluents giving lower counts than those obtained with distilled water. When seven species of yeast were enumerated in pure culture, highest counts were obtained using 0.1% peptone as the diluent and, with three exceptions, all species gave higher counts when diluted in diluents other than distilled water. When yeast suspensions were held in diluents for up to 2 h before plating, cell death occurred. The extent of death was highest in distilled water, saline and phosphate buffer diluents. Cell death also occurred in 0.1% peptone, yeast extract and malt extract, but to a lesser degree.

Beverages↗
PubMed1982

Appearance of a cell surface antigen associated with the activation of peritoneal macrophages in mice.

A relatively large population of murine peritoneal exudate macrophages induced with viable BCG or heat-killed Corynebacterium parvum was stained by the antiserum prepared against purified gangliotetraosyl ceramide (asialo GM1), while only a small population of peritoneal resident macrophages or peritoneal exudate macrophages induced with proteose peptone was stained. The cytotoxicity assay of those macrophages with anti-asialo GM1 plus complement supported these results. Peritoneal macrophages induced with BCG or C. parvum showed strong cytotoxicity for EL4 cells in vitro, while resident or peptone-induced peritoneal macrophages showed no cytotoxicity. BCG- or C. parvum-induced peritoneal cells contained both NK cells and cytotoxic macrophages, and either in vivo or in vitro pretreatment of the cells with anti-asialo GM1 and complement abolished the activities of both types of cells. Peptone-induced peritoneal macrophages incubated with lymphokines (LK) or lipopolysaccharide (LPS) were cytotoxic for EL4 cells and contained an increased number of cells stained by anti-asialo GM1. The cytotoxicity of these in vitro activated macrophages was reduced by treatment with anti-asialo GM1 plus complement. When peptone-induced peritoneal macrophages were incubated with LK, the number of cells stained by anti-Ia antiserum increased, but the number did not increase when the macrophages were incubated with LPS. Pretreatment of peptone-induced macrophages with anti-asialo GM1 plus complement did not affect the ability of the macrophages to be activated by LK. These results taken together strongly suggest that the antigen(s) reactive with anti-asialo GM1 is expressed on the cell surface of cytotoxic peritoneal macrophages in mice.

Animals↗
PubMed1982

The Microaerophile SPirillum volutans: Cultivation on Complex Liquid and Solid Media.

Spirillum volutans grows only under microaerobic conditions in a peptone-succinate-salts broth, but can grow aerobically when the peptone is replaced by vitamin-free acid-hydrolyzed casein broth. The addition of potassium metabisulfite, norepinephrine, catalase or superoxide dismutase (SOD) permitted aerobic growth in peptone-succinate-salts broth. A combination of catalase and SOD had a synergistic effect. S. volutans lacked catalase and had only a low level of peroxidase activity, but did possess SOD activity (12 to 14 U/mg of protein). The organism was found to be extraordinarily sensitive to exogenous hydrogen peroxide. Illumination of peptone-succinate-salts broth generated hydrogen peroxide and rendered the medium inhibitory to growth. A combination of catalase and SOD prevented this inhibition. Growth of S. volutans on solid media, not previously possible, was accomplished by the use of vitamin-free acid-hydrolyzed casein and peptone-succinate-salts agar media; maximum growth responses were dependent on the following combination of factors: addition of bisulfite, catalase, or SOD, protection of the media from illumination, incubation in a highly humid atmosphere, and incubation under atmospheres of 12% oxygen or less. The results indicate that the microaerophilic nature of S. volutans is attributable largely to the high sensitivity of the organism to exogenous hydrogen peroxide and, to a lesser extent, superoxide radicals occurring in the culture medium.

Journal Article↗
PubMed1988

Enrichment for Plesiomonas shigelloides from stools.

Bile peptone broth and alkaline peptone water (pH 8.5) were examined as enrichment media for the isolation of Plesiomonas shigelloides from stools, with salmonella-shigella agar as the isolation medium. After 423 parallel examinations in two different experiments, bile peptone broth enrichment for 24 h was observed to be six times more effective (P less than 0.01) than direct plating alone on salmonella-shigella agar. Bile peptone broth was found to be twice as effective as alkaline peptone water for the recovery of P. shigelloides from stools.

Culture Media↗
PubMed1992

Role of gastrin, histamine, and acetylcholine in the gastric phase of acid secretion in anesthetized rats.

To determine the relative contributions of gastrin, histamine, and cholinergic stimulation to the gastric phase of acid secretion, peptone-stimulated acid output was measured in urethan-anesthetized pylorus-ligated rats after intravenous administration of gastrin monoclonal antibody, cimetidine, and atropine. Intragastric peptone stimulated acid secretion four-fold over basal, which was associated with a significant increase in plasma gastrin levels. Gastrin immunoneutralization and simultaneous H2- and muscarinic-receptor blockade demonstrated that approximately 40% of peptone-stimulated acid output as attributed to endogenous gastrin through a histamine-dependent pathway, whereas 20% of acid output was accounted for by a cholinergic component. Another 10% of titratable acid was omeprazole-insensitive and presumably due to intragastric digestion of peptone. Therefore, approximately 30% residual acid output in response to peptone could not be accounted for by known acid stimulatory mechanisms. In rats given somatostatin monoclonal antibody to block the tonic inhibitory effect of endogenous somatostatin, residual acid output was a similar fraction of meal-stimulated acid output. In contrast, gastric distension induced by intragastric instillation of saline stimulated acid secretion to 1.5-fold over basal. Although 60% of distension-induced acid secretion could be inhibited by either H2 blockade or gastrin immunoneutralization, acid output returned to basal levels after simultaneous muscarinic blockade. These results indicate that gastrin, through a histaminergic pathway, is the principal mediator of meal-stimulated acid secretion in anesthetized rats. Approximately 30% of acid output was due to other unidentified mechanisms, such as chemical secretagogues, a direct effect of amino acids, or novel peptides.

Acetylcholine↗
PubMed1989

Retardation of articular cartilage degradation by glycosaminoglycan polysulfate, pentosan polysulfate, and DH-40J in the rat air pouch model.

The rat subcutaneous air pouch model was adapted to examine the in vivo degradation of implanted rabbit articular cartilage, both with and without induced air pouch inflammation, over a 7-day period. The effects of 3 drugs, glycosaminoglycan polysulfate (Arteparon), pentosan polysulfate (SP-54), and zinc-chelated pentosan polysulfate (DH-40J), on inflammation-induced cartilage degradation were also examined. Implanted articular cartilage from noninflamed air pouches showed a reduction in total proteoglycan (PG) content (as hexuronic acid), but not in PG extractability or aggregation, compared with cartilage maintained in tissue culture. The injection of peptone into the air pouch as an inflammogen caused an influx of leukocytes and plasma exudate and a reduction in implanted articular cartilage PG content, extractability, and aggregation, which was significantly greater than that which occurred in noninflamed air pouches. In vitro experiments demonstrated that peptone did not have a direct effect on cartilage PG degradation. Daily injection of Arteparon, SP-54, or DH-40J (10 mg/kg) into peptone-inflamed air pouches significantly increased the PG content, extractability, and aggregation in implanted articular cartilage, compared with that in cartilage from non-drug-treated control animals. The infiltration of leukocytes into the peptone-inflamed air pouches was significantly reduced by daily administration of Arteparon, 10 mg/kg. At an equivalent dose, DH-40J increased leukocyte numbers in the pouch fluid, whereas SP-54 had no significant effect on leukocyte accumulation.

Animals↗
PubMed1991

Inhibition of meal-stimulated gastric acid secretion by gastrin immunoneutralization in rats.

Gastrin 17-I was infused into conscious rats equipped with jugular and portal vein catheters and with a pyloric gastric drainage tube to achieve serum concentrations slightly higher than those found during intragastrically instilled peptone solutions. I.v. injected rabbit gastrin antiserum abolished gastrin 17-I-stimulated gastric acid secretion in these animals. Gastrin immunoneutralization reduced peptone-stimulated gastric acid secretion by approximately 37% during the entire 30-min period of stimulation. Peptone-stimulated gastric acid secretion was only significantly (P less than 0.05) inhibited in the third 10-min period, but not in the first or second 10-min periods of stimulation. This study demonstrates that the late but not the initial period of peptone-stimulated gastric acid secretion is regulated by circulating gastrin in rats.

Animals↗
PubMed1990

Stimulatory effect of pancreastatin on gastric acid secretion in conscious dogs.

Pancreastatin, a new 49-amino acid peptide, has recently been isolated and characterized from extracts of the porcine pancreas. The objective of the present study was to examine the effect of various doses of pancreastatin on gastric acid secretion in conscious dogs that were prepared with chronic gastric cannulas. Pancreastatin, administered IV at 400 pmol.kg-1 x h-1, enhanced peptone meal [peptone (5%), phenylalanine (90 mmol/L), glucose (12 g/dL)]-stimulated gastric acid secretion by 50%; pancreastatin at 800 pmol.kg-1 x h-1 enhanced peptone meal secretion by 165% (P less than 0.05). Intravenous administration of pancreastatin did not affect basal or peptone-stimulated release of gastrin. In addition, IV pancreastatin (400 pmol.kg-1 x h-1) failed to influence basal gastric acid secretion. Pancreastatin did not affect acid secretion stimulated by 2-deoxyglucose, histamine, or pentagastrin. The present study shows that pancreastatin can selectively enhance gastric acid secretion by a mechanism independent of cholinergic, histaminergic, or gastrin input.

Animals↗