Gastric Histamine Release Research Articles

Effects of the Histamine 1 Receptor Antagonist Cetirizine on the Osteoporotic Phenotype in H(+) /K(+) ATPase Beta Subunit KO Mice.

Epidemiological studies suggest increased fracture risk in patients using proton pump inhibitors (PPIs). We have previously shown that the H(+) /K(+) ATPase beta subunit knockout (KO) mouse, which is a model of PPI-use, have lower bone mineral density (BMD) and impaired bone quality compared to wild type (WT) mice. Like PPI users, these KO mice display elevated gastric pH and hypergastrinemia, which in turn stimulates gastric histamine release. Previous studies have suggested a negative effect of histamine on bone, thus, we wanted to study whether a histamine 1 receptor (H1R) antagonist could improve bone quality in KO mice. Female KO and WT mice aged 8 weeks received either an H1R antagonist (cetirizine) or polyethylene glycol (PEG) for 6 months. At the end of the study, KO mice displayed elevated plasma histamine levels compared to WT. As demonstrated previously, the KO mice also exhibited lower whole body BMD, reduced mechanical bone strength, and impaired bone quality assessed by μCT. No significant differences, however, were found between the KO groups receiving cetirizine or PEG for any of the measured bone parameters. In vitro gene expression analyses of histamine receptors revealed the presence of H1R and H2R both in osteoblasts and osteoclasts, and H3R in late stage osteoblasts. In conclusion, administration of the H1R antagonist cetirizine in a concentration of 3 mg/kg did not rescue the osteoporotic phenotype in H(+) /K(+) ATPase beta subunit KO mice. It can, however, not be ruled out that histamine may influence bone via other receptors. J. Cell. Biochem. 117: 2089-2096, 2016. © 2016 Wiley Periodicals, Inc.

64-Year-Old Woman With Diarrhea and Increased Abdominal Girth

64-year-old woman presented to our institution for evaluation of diarrhea and increasing abdominal girth. She had a 1-month history of postprandial diarrhea unrelated to the type of foods she consumed. Her stool was watery, with no evidence of gastrointestinal bleeding. Concurrently, she also noted increasing abdominal girth requiring new pants with a larger waist size. She had no abdominal pain, nausea/vomiting, flushing, light-headedness, or constitutional symptoms. Her medical history was notable for a previous stroke with a mild residual right hand tremor. She was a lifetime nonsmoker, had no history of illicit drug use, and drank alcohol rarely. She had no history of recent travel, infectious exposures, new medications, or herbal supplement intake. Her blood pressure was 136/83 mm Hg, and herheart rate was 98beats/min.Heroxygensaturation was 95% while she breathed room air, and her respiratory rate was 18 breaths/min. Her temperature was 36.9C. Her mental status was normal. Her abdomen was soft, nontender, and mildly distended with hyperactive bowel sounds. Shifting dullness with a fluid wave was present. 1. Which one of the following is the most appropriate diagnostic approach to evaluate the patient’s abdominal symptoms? a. Paracentesis b. Colonoscopy c. Clostridium difficile toxicology screen or polymerase chain reaction d. Serology testing for transglutaminase antibody e. Abdominal radiography

Importance of histamine, glutathione and oxyradicals in modulating gastric haemorrhagic ulcer in septic rats.

1. The ulcerogenesis of gastric haemorrhagic damage during sepsis is unclear. The present study first proposes that gastric haemorrhagic ulcer is modulated by mucosal glutathione, histamine and oxyradicals in lipopolysaccharide (LPS)-induced sepsis in rats. The protective effects of several drugs on the ulcerogenic parameters also were evaluated. 2. Male specific pyrogen-free Wistar rats were deprived of food for 24 h. For the induction of sepsis, intravenous LPS (0, 1, 3 or 10 mg/kg in 1 mL sterilized normal saline) was challenged to rats 12 h after withdrawal of food. Rat stomachs were vagotomized, followed by irrigation for 3 h with normal saline or a physiological acid solution containing 100 mmol/L HCI and 54 mmol/L NaCl. 3. The aggravation of gastric ulcerogenic parameters, such as gastric acid back-diffusion, luminal haemoglobin content, mucosal lipid peroxide production, histamine concentration, as well as lowered concentrations of defensive substances, including mucosal glutathione, were dependent on the doses of LPS used for challenge. A high correlation was observed between mucosal histamine release and lipid peroxide production in LPS rats. 4. The ulcerogenic parameters obtained in LPS (3 mg/kg, i.v.) rats were potently attenuated by diamine oxidase, ketotifen and zinc sulphate. 5. Several oxyradical scavengers, including glutathione, dimethylsulphoxide and allopurinol, also were effective in inhibiting haemorrhagic ulcer. 6. In conclusion, gastric mucosal histamine release and oxyradical generation play pivotal roles in the formation of haemorrhagic ulcers in septic rats.

Water Extracts of Helicobacter pylori Suppress the Expression of Histidine Decarboxylase and Reduce Histamine Content in the Rat Gastric Mucosa

Background: Acute Helicobacter pylori (Hp) infection in humans may be associated with markedly reduced gastric acid secretion, but the mechanism of this hypochlorhydria has not been fully explained. Aims: This study was designed to investigate how water extracts (WE) of Hp applied on rat gastric mucosa affect gastric secretion and mucosal histamine concentration as well as the gene expression for histamine decarboxylase (HDC), the key enzyme converting histidine to histamine and for interleukin-1β (IL-1β), the important proinflammatory cytokine. Materials and Methods: Wistar rats were surgically equipped with small cannulas to form gastric fistulas (GF). Four weeks after formation of GF, rats received either saline (control group) or WE obtained from type I Hp strain expressing CagA/VacA proteins and from type II Hp strain negative for CagA/VacA. Hp-WE was applied intragastrically (i.g.) in a volume of 1 ml at days 0, 2, 4 and 6 (total 4 times). At days 7 and 14, the secretory tests were performed during which basal gastric acid and pepsin secretion was examined and acid and pepsin outputs were measured. After secretory tests, the rats were sacrificed, the stomachs removed and the damage to the gastric mucosa was assessed by measuring the lesion area planimetrically and by histology, the gene expression in gastric mucosa for HDC and interleukin-1β (IL-1β) was analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) and Southern blot. Additionally, somatostatin concentration in gastric juice, gastric mucosal histamine content and plasma gastrin and IL-1β levels were determined using radioimmunoassay (RIA). Results: Administration of Hp-WE failed to induce gross mucosal damage but microscopic examination revealed partial denudation of gastric surface epithelium without causing deep necrosis. In secretory tests, Hp-WE produced marked hypochlorhydria but type I Hp-WE induced significantly stronger inhibition of acid and pepsin secretion than type II Hp-WE, both at days 7 and 14. Both, type I and type II Hp-WE suppressed significantly the gene expression for HDC mRNA and lowered significantly gastric mucosal histamine content as compared to respective values in vehicle-treated control gastric mucosa. Furthermore, Hp-WE, resulted in a significant increase in expression of IL-1β mRNA and a significant fall in luminal somatostatin concentration as well as a insignificant elevation of plasma gastrin level, the type I Hp-WE being more effective in these alterations than type II Hp-WE. Conclusions: (1) Ability of Hp-WE to induce superficial damage, the reduction in HDC mRNA and accompanying fall in gastric histamine release, contribute, at least in part, to marked hypochlorhydria observed in the stomach exposed to repeated Hp-WE treatments, and (2) the deleterious effect of Hp-WE on the gastric mucosa involves an impairment of gastrin-somatostatin link possibly resulting from the action of Hp-derived toxins and the induction in mucosal cells of proinflammatory cytokine such as IL-1β.

Gastric submucosal microdialysis: a method to study gastrin- and food-evoked mobilization of ECL-cell histamine in conscious rats

Rat stomach ECL cells are rich in histamine and chromogranin A-derived peptides, such as pancreastatin. Gastrin causes the parietal cells to secrete acid by flooding them with histamine from the ECL cells. In the past, gastric histamine release has been studied using anaesthetized, surgically manipulated animals or isolated gastric mucosa, glands or ECL cells. We monitored gastric histamine mobilization in intact conscious rats by subjecting them to gastric submucosal microdialysis. A microdialysis probe was implanted into the submucosa of the acid-producing part of the stomach (day 1). The rats had access to food and water or were deprived of food (48 h), starting on day 2 after implantation of the probe. On day 4, the rats received food or gastrin (intravenous infusion), and sampling of microdialysate commenced. Samples (flow rate 1.2 μl min −1) were collected every 20 or 60 min, and the histamine and pancreastatin concentrations were determined. The serum gastrin concentration was determined in tail vein blood. Exogenous gastrin (4-h infusion) raised microdialysate histamine and pancreastatin dose-dependently. This effect was prevented by gastrin receptor blockade (YM022). Depletion of ECL-cell histamine by α-fluoromethylhistidine, an irreversible inhibitor of the histamine-forming enzyme, suppressed the gastrin-evoked release of histamine but not that of pancreastatin. Fasting lowered serum gastrin and microdialysate histamine by 50%, while refeeding raised serum gastrin and microdialysate histamine and pancreastatin 3-fold. We conclude that histamine mobilized by gastrin and food intake derives from ECL cells because: 1) Histamine and pancreastatin were released concomitantly, 2) histamine mobilization following gastrin or food intake was prevented by gastrin receptor blockade, and 3) mobilization of histamine (but not pancreastatin) was abolished by α-fluoromethylhistidine. Hence, gastric submucosal microdialysis allows us to monitor the mobilization of ECL-cell histamine in intact conscious rats under various experimental conditions not previously accessible to study. While gastrin receptor blockade lowered post-prandial release of ECL-cell histamine by about 80%, unilateral vagotomy reduced post-prandial mobilization of ECL-cell histamine by about 50%. Hence, both gastrin and vagal excitation contribute to the post-prandial release of ECL-cell histamine.

Modulation of pentagastrin-induced histamine release by histamine H3 receptors in the dog.

The histamine H3 receptor has been shown to inhibit pentagastrin-induced gastric acid secretion in dogs. Since pentagastrin releases histamine in dogs, we have now assessed whether the effects of H3-receptor ligands may be indirectly mediated by changes in gastric histamine release. Pentagastrin infusions (1 or 6 micrograms/kg/h), alone or together with the H3-receptor agonist (R) alpha-methylhistamine (1.2 mumol/kg/h) or the antagonist thioperamide (0.1 mumol/kg/h), were performed in dogs. One group (anaesthetized) was used for enzyme immunoassays of plasma histamine and, when required. (R) alpha-methylhistamine in the gastrosplenic vein, and another group (non-anaesthetized) for measurement of gastric acid secretion. Histamine levels were increased five- and eight-fold after 1 and 6 micrograms/kg/h pentagastrin, respectively, whereas acid output was nearly maximal at the lower dosage. (R) alpha-methylhistamine, at a plasma concentration of 0.15 microM, inhibited histamine release by 78% (P < 0.007) and 37% (not significant) and the total acid output by 44% (P < 0.05) and 19% (not significant) after infusion of 1 and 6 micrograms/kg/h pentagastrin, respectively. Thioperamide, together with pentagastrin in low dose, significantly increased histamine release by 212% (P < 0.05), whereas acid output increased by 34% (not significant). The histamine H3 receptor mediates a negative feedback control of pentagastrin-induced release of gastric histamine. It is tonically activated by endogenous histamine after pentagastrin in low dosage. The control of acid secretion by the H3 receptor seems to involve modulation of endogenous histamine release, possibly by means of enterochromaffin-like cells.

The role of gastric histamine release in the acid secretory response to pentagastrin and methacholine in the dog

We have previously demonstrated that both pentagastrin and methacholine can stimulate histamine release from the canine stomach during short term administration of the secretagogues into the gastrosplenic artery. In this study we tested the hypothesis that gastric histamine release determines the acid secretory response to acid secretagogues. Increasing doses of pentagastrin (2, 6, and 20 ng/kg/min) and methacholine (0.1, 0.3, and 1 micrograms/min) were infused into the gastrosplenic artery in dogs, while gastric acid output, histamine and N tau-methyl histamine secretory rates were monitored. Histamine and N tau-methyl histamine concentrations in plasma were measured using GC/NICI-MS. Increasing doses of pentagastrin resulted in increasing gastric output. Total histamine secretory rate expressed as the sum of histamine and N tau-methyl histamine secretory rate showed a significant increase above basal with the two highest doses of pentagastrin. Regression analysis correlating the dose of pentagastrin to gastric acid output gave a correlation coefficient of 0.586 which was very significant. Regression analysis correlating the total histamine secretory rate to acid output gave a correlation coefficient of 0.498 which was also very significant. Increasing doses of methacholine also resulted in a dose-dependent increase in acid output. Histamine secretory rates showed a statistically significant increase above basal only at the 1 microgram/min infusion rate, however, the total histamine secretory rates (histamine + N tau-methyl histamine) were no longer significant at any of the doses of methacholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of cionin on histamine and acid secretion by the perfused rat stomach.

The protochordean octapeptide cionin is structurally a hybrid of mammalian cholecystokinin (CCK) and gastrin. An earlier study has shown that cionin in mammals stimulates gallbladder contraction and gastric somatostatin release, similarly to CCK-8. In the present study we examined the effect of cionin on histamine release and acid secretion of the stomach, both effects being mediated by CCK-B/gastrin receptors. Cionin induced a concentration-dependent increase in histamine release and acid secretion in the isolated, vascularly perfused rat stomach, detectable at a concentration of 4 pM and reaching a maximum at a concentration of 512 pM. The CCK-B/gastrin receptor antagonist L 365,260 abolished the stimulating effect of cionin on both histamine release and acid secretion, whereas the CCK-A receptor antagonist L 364,718 only had a faint effect. Cionin is a potent and efficient stimulator of gastric histamine release and acid secretion interacting via a CCK-B receptor.

Calcium mediates gastrin-induced gastric histamine release in the rat

This study examined the second messenger system responsible for gastrin-induced histamine release from the rat stomach. We examined the effect of different concentrations of ionized calcium, the calcium-channel blockers verapamil and nicardipine, and the intracellular calcium-chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester (BAPTA/AM) on gastrin-stimulated histamine release in the totally isolated vascularly perfused rat stomach. Moreover, the effect on baseline histamine release of caffeine as well as of forskolin and 3-isobutyl-1-methylxanthine (IBMX) was tested. Gastrin induced an immediate 10- to 15-fold increase in venous histamine. Perfusate ionized calcium in the 0.25-1.25 mM range did not affect histamine release; histamine release was attenuated by the 0.00 and 1.75 mM calcium concentrations. Verapamil, nicardipine, and BAPTA/AM inhibited gastrin-stimulated histamine release. Caffeine stimulated the release, whereas forskolin and IBMX had no effect. We conclude that gastrin-induced histamine release from the rat stomach is mediated by calcium, probably both from the intracellular pool and by transmembrane flux from the extracellular space.

The role of gastric secretagogues in regulating gastric histamine release in vivo

The effect of short-term intragastric arterial infusion of pentagastrin and methacholine on histamine and Nτ-Methyl histamine secretory rates was evaluated in mongrel dogs in vivo. Doses of pentagastrin and methacholine were chosen that stimulate gastric acid secretion equivalently. Histamine and Nτ-Methyl histamine secretory rates were evaluated by measuring the arterial and gastric venous plasma histamine and Nτ-Methyl histamine concentrations at several time points during the secretagogue infusion, and gastric blood flow was continuously monitored. Histamine and Nτ-Methyl histamine plasma concentrations were analyzed by stable isotope dilution technique using gas chromatography/ negative ion-chemical ionization mass spectrometry. Histamine and Nτ-Methyl histamine secretory rates were calculated by subtracting the arterial from the venous plasma concentrations and multiplying the difference by gastric plasma flow. Infusion of pentagastrin resulted in large pulsed increase of histamine release from 1.5 ± 0.7 ng/min at time 0 to 72 ± 20 ng/min at 5 minutes, which decreased to a plateau of 20 ± 8 ng/min at 20 minutes. Nτ-Methyl histamine secretory rate increased from 6.7 ± 1.9 ng/min at baseline to a maximum of 42.5 ± 13.1 ng/min at 10 minutes, and the increase was maintained for the duration of the pentagastrin infusion. Methacholine infusion was associated with a small but sustained increase in histamine release, from a baseline of 1.6 ± 0.6 ng/ min to 5.9 ± 1.7 ng/min at 5 minutes. Nτ-Methyl histamine secretory rate was unchanged by methacholine. Gastric blood flow changes to pentagastrin roughly paralleled the extent of histamine release, but methacholine is a gastric vasodilator in its own right. Our data indicate that pentagastrin is a much more effective stimulator of gastric histamine release than methacholine and that the overall role of histamine in gastrin-stimulated acid output is likely to be different from the role of histamine in cholinergic-mediated gastric acid output.

CCK-B (gastrin) receptor regulates gastric histamine release and acid secretion

To study the interdependence between gastric histamine release and acid secretion, we examined the effects of gastrin-(1-17) [G-(1-17)] or cholecystokinin-(1-33) [CCK-(1-33)] alone or combined with the gastrin (CCK-B) antagonist L365,260 or the CCK-A antagonist L364,718 in the isolated vascularly perfused rat stomach. G-(1-17) and CCK-(1-33) gave concentration-dependent increases in acid secretion and histamine release. Gastrin or CCK-A antagonist alone did not stimulate histamine release or acid secretion. Maximally G-(1-17) or CCK-(1-33) stimulated histamine release and acid secretion was unchanged by the CCK-A antagonist, while the gastrin antagonist induced a parallel and concentration-dependent decrease in stimulated histamine and acid secretion. We conclude that G-(1-17) and CCK-(1-33) stimulate histamine and acid secretion by a CCK-B (gastrin) receptor. The present results indicate that gastrin, at least in this species, stimulates acid secretion by releasing histamine.

Session 4: Aspects of the Regulation of Gastric Histamine Release

Histamine is found in large amounts in the gastric mucosa and plays an essential role in the regulation of acid secretion. It is thought to stimulate acid secretion directly after being released by the other two major secretagogues (gastrin and acetylcholine) (the mediator hypothesis) or to potentiate the action of the other two secretagogues (the interaction hypothesis). Recent studies with isolated, vascularly perfused rat stomach have shown that gastrin in physiologic concentrations elicits a release of histamine sufficient to explain its acid-stimulatory effect. Vagal nerve stimulation, on the other hand, only gives a faint histamine release, indicating that the vagal acid stimulation is mainly mediated by a direct stimulation of the parietal cell. Furthermore, the gastrin-stimulated histamine release seems to be mediated by a calcium-dependent mechanism. Somatostatin inhibits gastrin-stimulated histamine release via a paracrine mechanism, and a prostaglandin E1 analogue (misoprostol) has been shown to be a potent inhibitor of base-line and gastrin-stimulated histamine release. These studies show that the modulation of histamine release may be a central regulatory mechanism of gastric acid secretion. Although these studies have been done in rats, there are indications that these results are of a general nature nd valid for other species as well.

Histamine release in the isolated vascularly perfused stomach of the rat: regulation by autoreceptors

1. In the isolated vascularly-perfused stomach of the rat, gastrin 1-17 (520 pmol 1(-1)) increased acid output from basal values of 13.7 +/- 2.7 to 92.5 +/- 11.4 mumol h-1 and venous histamine output from 10.1 +/- 2.3 to 54.7 +/- 7.9 nmol h-1 (mean +/- s.e.mean). 2. The H1 receptor agonist 2-methylhistamine (10 mumol 1(-1)) increased acid output to 21.6 +/- 2.9 mumol h-1 (P less than 0.05) and reduced basal histamine output to 4.0 +/- 0.8 nmol h-1 (P less than 0.05). Gastrin-stimulated acid secretion and vascular histamine output was not significantly affected by 2-methylhistamine (10 mumol 1(-1)). 3. The H2 receptor agonist, impromidine, dose-dependently increased basal acid secretion, reaching a maximal value of 145.5 +/- 11.7 mumol h-1 with impromidine (10 mumol 1(-1)), and maximal gastrin-stimulated acid secretion to 167.4 +/- 15.1 mumol h-1 with impromidine (10 mumol 1(-1)). Impromidine dose-dependently inhibited basal and gastrin-stimulated vascular histamine output. 4. The H3 receptor agonist R-a-methylhistamine, (1 and 10 mumol 1(-1)) minimally increased basal acid secretion. R-a-methylhistamine (10 mumol 1(-1)) did not significantly affect maximal gastrin-stimulated acid secretion. Basal and gastrin-stimulated vascular histamine outputs decreased to 4.0 +/- 0.8 (P less than 0.05) and 24.7 +/- 4.7 nmol h-1 (P = 0.05) with R-a-methylhistamine (10 mumol 1(-1)). 5. The H2 receptor antagonist ranitidine (2 mumol 1(-1)) did not inhibit basal acid secretion, but acid outputs with gastrin and all histamine agonists were reduced. Ranitidine did not affect histamine release in the basal state, with gastrin or with any histamine agonist tested. 6 We conclude that gastric histamine release in the rat is regulated via a histamine H2 receptor sensitive to the histamine agonists tested, but not to ranitidine. It is unlikely that the inhibition of histamine release is secondary to increased gastric acidity.

Inhibitory effect of isoprenaline on gastric acid secretion in the rat. The role of endogenous histamine

In dogs beta-adrenoreceptor agonists inhibit gastric acid secretion stimulated by exogenous gastrin to a much greater extent than acid secretion stimulated by exogenous histamine. One possible explanation for this observation is that endogenous histamine is important in gastrin-mediated acid secretion and that isoprenaline and related beta-adrenoreceptor agonists block gastric mucosal histamine release. This possibility was tested in the present study in gastric lumen-perfused anaesthetized rats. Intravenous infusion of isoprenaline (12 microgram kg-1 h-1) inhibited maximal, pentagastrin-stimulated acid output by 50-70% (P less than 0.01), but had no significant inhibitory effect on the maximal acid secretory response to histamine. In contrast to its inhibitory effect on gastrin-stimulated acid output, isoproterenol had no effect on gastric histamine output during pentagastrin infusion. We conclude that isoprenaline selectively inhibits gastrin-stimulated acid secretion in the rat, as in the dog, and by a mechanism other than inhibiting gastric histamine release.

The effect of protamine sulfate on gastric acid secretion and histamine release.

１. Gastric acid secretion (GAS) of rats was dose-dependently increased by intravenous injection of 10-40 mg/kg protamine sulfate (PS). The frequency of occurrence vs. total acid output induced by each injection of PS (20 mg/kg) reavealed a statistical lognormal distribution in 65 rats. ２. Treatment with pyrilamine (5mg/kg, i.p.) or diphenhydramine (5 mg/kg, i.p.) 30 min before the injection of PS failed to inhibit the protamineinduced gastric secretion (PIGAS). However, atropine (5 mg/kg), cromolyn sodium (10mg/kg, i.p.) of cimetidine (2 mg/kg, i.p.) inhibited this effect. ３. Acid secretion and histamine-release from isolated bullfrog gastric mucosal preparations were measured in vitro by a recording pH stat and fluorometric asay. PS (2×10-4g/ml)increased GAS and histamine-release in a mucosal solution and serosal solution respectively. After the spontaneous secretion was decreased by treatment with cimetidine (1×10-4g/ml)and washed with serosal solution. Further application of PS restored acid secretion and histamine-release. ４. It is concluded that PS induces histamine-release (both in vivo and in vitro) from histamine-containing cells, basophil leucocytes and mast cells, and thereafter stimulates the acid secretion from parietal cells.

The aetiology of gastric ulceration induced by electrical vagal stimulation in rats

Histamine and serotonin levels in gastric secretion and the effects of pharmacological antagonists were studied in rats in which stomach ulceration was induced by electrical vagal stimulation. Electrical vagal stimulation (2 and 5 V) produced a graded increase in haemorrhagic glandular mucosal ulcers. NaHCO 3 perfusion completely neutralised the increased acid output but failed to prevent ulceration. Atropine inhibited gastric mast cell degranulation as well as histamine and serotonin release. Diphenhydramine, atropine and sub-diaphragmatic vagotomy antagonised the increase in intragastric pressure. Diphenhydramine, cimetidine, atropine or vagotomy but not methysergide reduced ulcer severity. It is concluded that gastric acid and serotonin do not play an important role in glandular ulceration induced by electrical vagal stimulation. The lesions probably result from increased intragastric pressure and release of gastric histamine which stimulates H 1 and H 2 receptors in the stomach. The similarities between the aetiologies of glandular ulcers due to electrical vagal stimulation and to stress are also discussed.

Release of gastric histamine in patients with urticaria and food allergy.

In a clinical study the participation of histamine in the allergenic response of patients with food allergy was investigated. The resting levels of gastric tissue and plasma histamines of 10 patients were slightly higher than the respective values of normal volunteers. 5 minutes after local intragastral allergenic provocation a decline of the mucosal histamine content of the allergen-treated area was noticed. Parallel investigations on the mast cell content of the stomach mucosa revealed a parallel decrease of the o-phthaldialdehyde stained cells, whereas the number of toluidine blue stained cells remained unchanged. These data are in accordance with an antigen-induced IgE-dependent liberation of the mast cell histamine stores.

The effects of zinc sulphate on gastric histamine release and ulcer formation in stressed pylorus-occluded rats

Summary Zinc sulphate (22, 44 or 88 mg/kg; given i.p. 48 h before experiments) reduces the histamine found in the gastric secretion of stressed pylorus-occluded rats; the incidence of gastric glandular ulcers, the secretory volume and the total acid output are also lowered. The dose-related changes are associated with increased histamine levels in the stomach wall. These findings imply a relationship between reduced gastric histamine release and ulcer prevention by zinc sulphate.

Colchicine inhibits stimulated release of gastric histamine but not activation of histidine decarboxylase.

In the rat, gastric mucosal histamine is mobilized and histidine decarboxylase activated by treatment with insulin or pentagastrin. Colchicine pretreatment prevented the histamine release without preventing the enzyme activation. The results suggest a) that histamine release and histidine decarboxylase activation are independent events, and b) that microtubules are involved in the release of histamine.

Pentagastrin and acetylcholine relation to histamine in H+ secretion by gastric mucosa.

ARTICLESPentagastrin and acetylcholine relation to histamine in H+ secretion by gastric mucosaDK Kasbekar, HA Ridley, and JG ForteDK Kasbekar, HA Ridley, and JG FortePublished Online:01 Apr 1969https://doi.org/10.1152/ajplegacy.1969.216.4.961MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe gastric parietal cell: at home and abroadEuropean Surgery, Vol. 42, No. 3An update on acid secretion20 January 2006Transient Increase of Blood Histamine Level Induced by Pentagastrin Continuous Monitoring by in vivo Microdialysis8 July 2009 | Scandinavian Journal of Gastroenterology, Vol. 31, No. 12Famotidine, a histamine-2-receptor antagonist, inhibits the increase in rat gastric H+/K+-ATPase mRNA induced by intravenous infusion of gastrin 17 and histamineDigestive Diseases and Sciences, Vol. 40, No. 9The role of gastric histamine release in the acid secretory response to pentagastrin and methacholine in the dogInflammation Research, Vol. 44, No. 8Inhibitory effect of DS-4574, a mast cell stabilizer with peptidoleukotriene receptor antagonism, on gastric acid secretion in ratsEuropean Journal of Pharmacology, Vol. 255, No. 1-3Antisecretory effect of DS-4574, a mast cell stabilizer with peptidoleukotriene antagonism, on gastric acid secretion in the pigAgents and Actions, Vol. 41, No. 1-2Pharmacology of gastric acid inhibitionBaillière's Clinical Gastroenterology, Vol. 7, No. 1The role of gastric secretagogues in regulating gastric histamine release in vivoGastroenterology, Vol. 102, No. 2Histamine and the Parietal CellFade and tachyphylaxis of gastric acid secretory response to pentagastrin in rat isolated gastric mucosa19 July 2012 | British Journal of Pharmacology, Vol. 95, No. 4Mechanisms of stimulation of acid production in parietal cells isolated from the pig gastric mucosaActa Physiologica Scandinavica, Vol. 131, No. 4Control of gastric secretionThe American Journal of Medicine, Vol. 83, No. 2Effects of cimetidine, atropine and pirenzepine on basal and stimulated gastric acid secretion in the ratEuropean Journal of Pharmacology, Vol. 138, No. 2Gastrin Produces an Immediate and Dose-Dependent Histamine Release Preceding Acid Secretion in the Totally Isolated, Vascularly Perfused Rat Stomach8 July 2009 | Scandinavian Journal of Gastroenterology, Vol. 22, No. 7Histamine: the sole mediator of pentagastrin-stimulated acid secretionActa Physiologica Scandinavica, Vol. 125, No. 1Histamine stimulation of digestive enzyme secretion byin vitro rabbit pancreasDigestive Diseases and Sciences, Vol. 27, No. 3Regulation of Gastric Acid SecretionHistamine Receptors and Gastric SecretionNonreplicating Cultures of Frog Gastric Tubular CellsGastrin - Histamine as a Normal Sequence in Gastric Acid Stimulation in the Rabbit18 January 2010 | Upsala Journal of Medical Sciences, Vol. 84, No. 2Potentiation by Carbachol and Aminophylline of Histamine- and db-cAMP-Induced Parietal Cell Activity in Isolated Gastric GlandsActa Physiologica Scandinavica, Vol. 99, No. 1Effects of Secretagogues on Oxygen Consumption, Aminopyrine Accumulation and Morphology in Isolated Gastric GlandsActa Physiologica Scandinavica, Vol. 97, No. 4INFLUENCE OF HISTAMINE RELEASING AGENTS ON GASTRIC ACID SECRETION OF ISOLATED BULLFROG GASTRIC MUCOSAJapanese Journal of Pharmacology, Vol. 26, No. 6Histamine release by gastric stimulantsNature, Vol. 253, No. 5486Adenyl cyclase of oxyntic cells its association with different cellular membranesBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 363, No. 3A phylogenetic study on the occurrence and distribution of histamine in the gastro-intestinal tract and other tissues of man and various animalsComparative and General Pharmacology, Vol. 4, No. 15Effects of Atropine on Acid Secretion by Isolated Frog Gastric MucosaGastroenterology, Vol. 62, No. 6STUDIES ON THE EFFECT OF HEMICHOLINIUM-3 ON GASTRIC ACID SECRETION IN THE ISOLATED BULLFROG GASTRIC MUCOSA WITH SPECIAL REFERENCE TO THE MODE OF ACTION OF GASTRIN-LIKE TETRAPEPTIDEJapanese Journal of Pharmacology, Vol. 20, No. 4 More from this issue > Volume 216Issue 4April 1969Pages 961-967 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.216.4.961PubMed5775893History Published online 1 April 1969 Published in print 1 April 1969 Metrics