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At least 19 recordsLinked to original sources
PubMed1988

Dietary linoleic acid, gastric acid, and prostaglandin secretion.

Basal and pentagastrin-stimulated gastric acid secretion, fasting serum gastrin concentrations, and the gastric output of prostaglandin E and its major metabolite 13,14-dihydro 15-keto prostaglandin E2 were measured in 9 normal subjects before and after 14-20 days of dietary supplementation with linoleic acid. Mean maximal gastric acid output fell from 36.0 +/- 3.3 (SEM) to 30.1 +/- 2.9 mmol/h (p less than 0.05), although mean basal acid output was not significantly affected (8.3 +/- 2.1 and 7.2 +/- 1.7 mmol/h, respectively). Mean fasting serum gastrin concentrations increased from 19.2 +/- 3.1 to 30.9 +/- 3.8 ng/L (p less than 0.01) after linoleic acid, probably because of acid suppression. The mean output of prostaglandin E increased from 498 +/- 110 to 1254 +/- 465 ng/h (p less than 0.05); that of its metabolite increased from 165 +/- 18 to 1168 +/- 645 ng/h (p less than 0.01). These findings show that in normal subjects essential fatty acid weakly inhibits gastric acid secretion, but considerably increases gastric prostaglandin output.

Adult↗
PubMed1975

Effect of optimum therapeutic dose of poldine on acid secretion, gastric acidity, gastric emptying, and serum gastrin concentration after a protein meal.

An oral optimum therapeutic dose of poldine was established in 5 normal subjects. Acid secretion in response to a protein meal was measured for 3 hr by continuous intragastric titration with sodium bicarbonate. Poldine 30 min before the meal reduced food-stimulated acid secretion from zero to 60% in the 5 subjects (average inhibition 32%). Poldine inhibited histamine-stimulated acid secretion to approximately the same extent. In separate experiments, gastric acidity after the meal was allowed to seek its natural level (i.e., there was notitration with bicarbonate). Poldine reduced average hydrogen concentration of the gastric contents by 85 to 50% from 1.5 to 3 hr after the meal. Since poldine did not alter the volume or the buffer content of the stomach, poldine inhibition of gastric acidity is due entirely to reduction of acid secretion and not to delayed emptying of food buffer. Poldine had no consistent effect on serum gastrin concentration after the meal when pH was maintained at a constant level by titration with bicarbonate; therefore, poldine inhibition of acid secretion is not mediated by a reduction of serum gastrin concentration.

Administration, Oral↗
PubMedDate not supplied

[Gastric Acid].

Gastric acid, a product of parietal cells secretion, full fills multiple biological roles which are absolutely necessary to keep corporal homeostasis. The production of the acid depends upon an effector cellular process represented in the first step by histamine, acetilcholine and gastrin, first messengers of the process. These interact with specific receptors than in sequence activate second messengers -cAMP and the calcium-calmodulin system- which afterwards activate a kinase. An specific protein is then phosphorilated by this enzyme, being the crucial factor that starts the production of acid. Finally, a proton bomb, extrudes the acid towards the gastric lumen. The secretion process mentioned above, is progressive lyactivated in three steps, two of which are stimulators -cephalic and gastric phases- and the other one inhibitor or intestinal phase. These stages are started by mental and neurological phenomena -thought, sight, smell or memory-; by food, drugs or other ingested substances; and by products of digestion. Changes in regulation of acid secretion, in the structure of gastro-duodenal mucosal barrier by a wide spectrum of factors and agents including food, drugs and H. pylori, are the basis of acid-peptic disease, entity in which gastric acid plays a fundamental role. From the therapeutic point of view, so at the theoretical as at the practical levels, t is possible to interfere with the secretion of acid by neutralization of some of the steps of the effector cellular process. An adequate knowledge of the basics related to gastric acid, allows to create strategies for the clinical handling of associated pathology, specifically in relation to peptic acid disease in all of the known clinical forms.

Acetylcholine↗
PubMed1976

Effect of a mixture of red pepper (Capsicum frutescens) and an amino-acid on gastric acid secretion.

The effects of a mixture of red pepper suspension and alpha-alanine (an amino-acid) on gastric acid secretion in 33 duodenal ulcer and 18 non-duodenal ulcer patients were studied. This mixture caused an increase of gastric acid in the two groups of patients, more so in the duodenal ulcer group (0.025 > P > 0.010). Compared with the results of previous studies the administration of alpha-alanine in red pepper suspension produced less gastric acid than the fresh red pepper suspension alone.

Adult↗
PubMed1992

Intestinal acid inhibits gastric acid secretion by neural and hormonal mechanisms in rats.

To determine the relative contributions of neural reflexes and intestinal hormones to the inhibition of gastric acid secretion by intestinal acidification, rats with an extrinsically denervated, transplanted segment of jejunum, and those with an innervated segment of jejunum, were studied. Postoperatively, meal-stimulated gastric acid secretion was measured. When the acid secretory response to intragastric liver extract reached a plateau, graded concentrations of hydrochloric acid or saline were instilled into the jejunal segments. Gastric acid secretion was inhibited by intrajejunal acid (pH 2.5) by 79% in the innervated rats and by 64% in the transplanted group. Thus at a pH of 2.5 there was a 15% greater maximum inhibition of plateau acid response in the innervated rats than in the transplanted rats, presumably because of the extrinsic neural contribution. To examine the hormonal mediators, the effects of a somatostatin monoclonal antibody and a CCK-A receptor antagonist (L 364718) on acid-induced inhibition of gastric acid secretion were studied in transplanted rats. Treatment with a somatostatin monoclonal antibody or with L 364718 reduced the acid-induced (pH 2.5) inhibition of gastric acid secretion by 93 and 27%, respectively. Jejunal acidification inhibits gastric acid secretion in the rat by both neural and hormonal mechanisms. The hormonal mechanism is mediated by somatostatin and CCK.

Acids↗
PubMed1970

Sex hormones, and acid gastric secretion induced with carbachol, histamine, and gastrin.

This study confirms previous reports that satisfactory gastric acid secretory responses to intravenous administration of histamine, carbachol, and gastrin can be obtained. Bilateral castration of the male rats significantly reduced acid gastric secretory responses to carbachol but not to histamine. Overiectomized rats treated with 17B-oestradiol (short-term treatment) showed a statistically significant reduction in gastric acid secretion induced with all the secretagogues, but the results when rats were treated with testosterone were inconsistent. In animals given gastrin or histamine gastric acid secretion was reduced and was of statistical significance with gastrin (0.02 < p < 0.05) but not with histamine (0.05 < p > 0.1). It is concluded that a high oestrogen blood level is capable of inhibiting effectively acid gastric secretion in both sexes except that a higher level of blood oestrogen is required in the male. The results showed further that of all the sex hormones used, only oestrogen had a significant effect on gastric acid secretion.

Animals↗
PubMed1992

Importance of gastric acid in gastric ulcer formation in rabbits with antibody-induced prostaglandin deficiency.

The role of gastric acid in the development of gastroduodenal ulcers in prostaglandin-deficient conditions is unclear. In the current study, the effect of the proton pump inhibitor omeprazole on the formation of gastric ulcers was examined in a previously validated rabbit model of antibody-induced prostaglandin deficiency. Intragastric administration of 20 mg/kg omeprazole every 12 hours caused a profound suppression of gastric acidity (i.e., pH above 5 continuously). This same dose of omeprazole significantly reduced gastric ulcer formation induced by passive immunization with 6-keto-prostaglandin F1 alpha antibodies. It is concluded from these observations that gastric acid plays a critical role in the formation of gastric ulcers in rabbits with antibody-induced prostaglandin deficiency.

6-Ketoprostaglandin F1 alpha↗
PubMed2004

Regulation of expression of the receptors controlling gastric acidity.

Gastric acid secretion is regulated by the stimulatory effects of gastrin, histamine and acetylcholine and the inhibitory actions of somatostatin on their respective receptors. We proposed that the expression of these receptors could be regulated at the transcription level by agonists and antagonists known to effect acid secretion. A quantitative "real-time" PCR method was used to determine changes in mRNA expression for these receptors. The agonists, pentagastrin and histamine, and the H2 antagonist, ranitidine, were infused over a 6 h period to conscious sheep. Blood, antral and fundic tissue samples were taken for analysis. Both pentagastrin and histamine resulted in elevated plasma somatostatin concentrations during the treatment. Ranitidine stimulated a fourfold increase in plasma gastrin while histamine caused a transient decrease. Except for an increase in antral gastrin following ranitidine infusion, there was no significant change in gastric gastrin and somatostatin concentration. Histamine (H2) receptor mRNA expression in the antrum was significantly increased by pentagastrin and decreased by ranitidine. Pentagastrin also stimulated a significant increase in the level of muscarinic (M3) receptor mRNA in the antrum. Antral somatostatin II receptor mRNA was significantly decreased by histamine. In the fundus, pentagastrin infusion resulted in a significant increase in histamine receptor mRNA and a decrease in the muscarinic receptor mRNA. This work demonstrates that the receptors involved in the regulation of acid secretion can be regulated by local events.

Animals↗
PubMed1990

Effects of FRG-8701 on gastric acid secretion, gastric mucosal lesions by necrotizing agents and experimental gastric or duodenal ulcer in rats.

Effects of FRG-8701, a new histamine H2-receptor antagonist, on gastric acid secretion, necrotizing agents-induced gastric lesions and acute gastric or duodenal ulcer in rats were studied. In lumen-perfused rats, intravenous injection of FRG-8701 reduced gastric acid secretion, and its antisecretory effect was almost equipotent to that of famotidine but the duration of action was substantially longer. In pylorus-ligated rats, the antisecretory effect of intraduodenal FRG-8701 administration was about 7 times more potent than that of cimetidine. FRG-8701 effectively inhibited macroscopic gastric hemorrhagic lesions induced by various kinds of necrotizing agents. Intraperitoneal injection was effective in preventing the lesions as well as oral treatment. The oral ED50 values for these lesions ranged from 1.1 to 9.4 mg/kg. On the other hand, famotidine failed to reduce these lesions, and the cytoprotective effect of cimetidine was observed only in high doses compared with the doses for antisecretory activity. In addition, the cytoprotective effect of FRG-8701 was not affected by the treatment of indomethacin or N-ethylmaleimide. FRG-8701 showed antiulcer activity against stress and indomethacin gastric ulcer and mepirizole duodenal ulcer. Its antiulcer effect was 5-15 times more potent than that of cimetidine. These results indicate that FRG-8701 is a new antiulcer drug that exerts a potent cytoprotective effect in addition to its gastric antisecretory activity.

Acetamides↗
PubMed2001

Four response stages of capsaicin-sensitive primary afferent neurons to capsaicin and its analog: gastric acid secretion, gastric mucosal damage and protection.

Capsaicin is the active component of red hot peppers, which modifies specifically the capsaicin-sensitive sensory afferent nerves. The action of capsaicin is an initial short-lasting stimulation, which is followed by desensitization to capsaicin itself, and to other stimuli of afferent sensory nerves. Four response stages of capsaicin-sensitive primary afferents exist to capsaicin, depending on the dose and duration of exposure to the drug. These are excitation, a sensory blocking effect, long-term selective neurotoxic impairment, and irreversible cell destruction. The possible roles of four stages of capsaicin-sensitive primary afferents can be evaluated in relation to gastric acid secretion, and to the details of the defensive side of gastric mucosa against different chemicals, physical agents, drugs and other pathological stress. Capsaicin inhibited the gastric acid secretion in pylorus-ligated rats when it was given intragastrically at a dose of 0.4-1.8 microg/kg. Small doses of capsaicin (up to 800 microg, i.g.) produced a dose-dependent inhibition (ID50 = 400 microg), and its inhibitory effect was exerted for 1 h in healthy human subjects. While a small dose (5 microg/kg) of capsaicin caused inhibition, a high dose (50-100 mg/kg) enhanced the gastric mucosal lesions productivity by causing hyperacidity in pylorus-ligated animals. Capsaicin and its analog inhibited the development of different chemically induced gastric mucosal damage in various experimental models if they were given intragastric doses (microg/kg). The final effects of capsaicin depend on the dosage and timing. The different effects are excitation, a sensory-blocking effect, long-term selective neurotoxic impairment and irreversible cell destruction.

Afferent Pathways↗
PubMed1982

Effect of individual l-amino acids on gastric acid secretion and serum gastrin and pancreatic polypeptide release in humans.

Individual l-amino acids were instilled intragastrically to determine possible differences in stimulation of gastric acid secretion and gastrin and pancreatic polypeptide release. Phenylalanine and tryptophan were significantly more potent stimulants of gastric acid secretion and of pancreatic polypeptide and gastrin release than any of the other amino acids tested. Smaller, but significant, responses were obtained with threonine for pancreatic polypeptide and with serine for acid secretion. We conclude that a major part of the acid-stimulating action of mixed amino acid solution can be explained by the aromatic amino acids, phenylalanine and tryptophan, which are also the most potent stimulants of gastrin and pancreatic polypeptide release. These studies suggest that the specific composition of amino acid mixtures determines the net effects of such mixtures on gastric secretion, and on release of both the antral hormone gastrin and the pancreatic hormone, pancreatic polypeptide.

Adult↗
PubMed1984

Effects of morphine, enkephalins and naloxone on postprandial gastric acid secretion, gastric emptying and gastrin release in dogs.

The effects of intravenous infusions of morphine, met-enkephalin and leu-enkephalin on gastric acid secretion, gastrin release and gastric emptying were investigated in four dogs with gastric cannulas stimulated by a liquid peptone meal. The actions of a potent opiate antagonist, naloxone, used alone or combined with opiates were also studied. Morphine, met-and leu-enkephalin decreased the fractional gastric emptying rate. Acid secretion was decreased by enkephalins and increased by high doses of morphine. Enkephalins and to a lesser degree morphine inhibited gastrin release during the first hour following the administration of the meal. Only leu-enkephalin decreases significantly the integrated gastrin response. Naloxone at the doses used antagonized partly or totally the effects of opiates on gastric emptying but not those on gastric secretion or gastrin release. Naloxone infused alone had no significant effect on the gastric functions tested. These studies indicate that in dogs stimulated by a liquid test meal, enkephalins inhibit gastric emptying, acid secretion and gastrin release. Morphine inhibits gastric emptying and gastrin release and enhances acid secretion.

Animals↗
PubMed1992

Effects of a prostacyclin analog, U-68,215, on gastric acid secretion, gastric emptying and systemic blood pressure in primates.

The effect of the prostacyclin analog U-68,215 on gastric function and systemic blood pressure was evaluated in a primate model. Starting 30 min after histalog (1 mg/kg s.c.), gastric acid secretion and gastric emptying were determined over a 30-min period using a 99mTc-diethylene triamine pentaacetic acid dilution technique. Each animal then received an intragastric bolus of 0, 25, 50 or 100 micrograms/kg of U-68,215 and, after a 30-min equilibration period, gastric function was determined for an additional 60 min (histalog + U-68,215). Systemic blood pressure and heart rate were measured periodically using a pressure cuff and a Korotkoff microphone. U-68,215 produced a 94% maximum suppression of acid output from 60 to 90 min after 100 micrograms/kg U-68,215. Gastric emptying was significantly inhibited by all doses of U-68,215, and no diarrhea was observed in response to any dose of U-68,215. Systolic blood pressure was significantly inhibited (P less than .05) only after the 100 micrograms/kg, whereas diastolic blood pressure was reduced significantly (P less than .05) by both 50 and 100 micrograms/kg and was positively correlated with acid secretion (r = .53; P less than .05). These data demonstrate that U-68,215 produces a significant inhibition of acid secretion without the stimulatory effect on gastric emptying induced by PGE analogs. Thus, prostacyclin analogs may represent an attractive alternative to PGE analogs in the treatment of peptic ulcer disease.

Animals↗
PubMed1991

gamma-Aminobutyric acid and gastric acid secretion: a physiologic role?

The purpose of this study was to examine the effect of endogenous brain GABA levels or GABAergic tone on gastric acid secretion. Experiments were performed with Sprague-Dawley rats under urethane anesthesia. Continuous acid secretion was measured in vivo using a gastric luminal perfusion system. Initial experiments studied the effects on basal acid secretion of (aminooxy)acetic acid (AOAA), a substance which increases brain GABA levels, and flumazenil, a substance which decreases central GABAergic neurotransmission. After basal acid secretion was measured for 30 min, AOAA (15 mg/kg), flumazenil (10 mg/kg), or saline was given by intravenous infusion and acid secretion was measured for 120 min. There was no significant difference in acid secretion between groups (n = 8/group). A second series of experiments measured the effects of AOAA, flumazenil, or saline on gastric secretion during submaximal stimulation by bethanechol (180 micrograms/kg/hr) in normal and vagotomized rats. Total acid secretions (mean +/- SE) after saline, AOAA, or flumazenil were 78.7 +/- 11.8, 51.0 +/- 5.9, and 109.3 +/- 1.5 mumole/90 min, respectively (P less than 0.01). In vagotomized rats, there were no significant differences in rates of acid secretion between groups. In summary, GABAergic tone did not effect basal acid secretion in anesthetized rats. However, during submaximal acid secretion, acid secretion decreased when brain GABA levels increased, and acid secretion increased when GABAergic neurotransmission was inhibited. We conclude that endogenous brain GABA levels may effect gastric acid secretion in rats, perhaps via inhibition of central-vagal tone.

Aminooxyacetic Acid↗
PubMed2003

Meal-stimulated gastric acid secretion and integrated gastric acidity in gastro-oesophageal reflux disease.

BACKGROUND: No current methods exist to determine meal-stimulated gastric acid secretion in humans under conditions that approximate those of daily living with the ingestion of breakfast, lunch and dinner. METHODS: Gastric and oesophageal pH were measured in 26 healthy subjects and in 59 subjects with gastro-oesophageal reflux disease. Meal-stimulated gastric acid secretion was calculated from the buffer capacity of the meals determined in vitro and from the time required for the gastric pH to decrease to pH 2 in vivo following ingestion of the meal. RESULTS: There was a significant correlation between gastric secretion with each meal and the corresponding post-prandial integrated gastric acidity. There was also a significant correlation between meal-stimulated gastric secretion and integrated gastric acidity from 09.00 to 22.00 h in both subjects with gastro-oesophageal reflux disease and controls. In subjects with gastro-oesophageal reflux disease, gastric secretion and integrated gastric acidity from 09.00 to 22.00 h were significantly higher than those in controls. There was a significant correlation between oesophageal acidity and integrated gastric acidity from 09.00 to 22.00 h in subjects with gastro-oesophageal reflux disease. CONCLUSIONS: As post-prandial gastric acidity is increased in subjects with gastro-oesophageal reflux disease, it seems likely that increased gastric acidity is an important aetiological factor in this disease.

2-Pyridinylmethylsulfinylbenzimidazoles↗