Hydrogen Ion Concentration in the Gastric Juice after Pylorus Ligation in Dexamethasone‐Treated Rat

Haikonen, M; Fäsänen, Toimi

doi:10.1111/j.1748-1716.1965.tb04288.x

Cited by 15 publications

(7 citation statements)

References 13 publications

(8 reference statements)

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“…After the dexamethasone treatment in the pyloric ligated rat stomach the acid secretion decreases but recovers after administration of lage amount of exogenous histamine (Rasanen and Haikonen 1965).…”

Section: Discussionmentioning

confidence: 95%

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Histidine Induced Secretion in the Pyloric Ligated Rat Stomach

Räsänen

1966

Acta Physiologica Scandinavica

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The amount and the pH of the gastric juice in the 1 hr pyloric ligated rat stomach were measured. The amount and the hydrogen ion concentration of the gastric juice were greater when the rats were injected with histidine than with histamine. The pretreatment with 5 times 1 mg of dexamethasone at 12‐hr intervals degranulated the mast cells of the gastric mucosa and increased the pH in the gastric juice. The difference of the secretory activity in histidine or histamine injected rats disappeared after the dexamethasone treatment. The results suggest that the gastric parenchyma is stimulated immediately with histamine formed from histidine and stored in the gastric mucosal mast cell organ.

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Section: Discussionmentioning

confidence: 95%

“…After the exhaustion of the gastric mucosal mast cell organ with dexamethasone the acid secretion in the pyloric ligated rat stomach decreases. The secretion can be restored, however, by giving a large amount of exogenous histamine (Rasanen and Haikonen 1965). I t has been observed that mast cell granules are rich in histidine decarboxylase (Schayer 1965).…”

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confidence: 99%

Histidine Induced Secretion in the Pyloric Ligated Rat Stomach

Räsänen

1966

Acta Physiologica Scandinavica

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“…Dexamethasone is a well known potent stimulator of gastric acid secretion [4,5]. The mechanisms underlying the stimulation of gastric acid secretion by dexamethasone are, however, a matter of controversy.…”

Section: Discussionmentioning

confidence: 99%

“…Glucocorticoids inhibit the inherent gastroprotective mechanisms of the stomach by inactivating the biosynthesis of prostaglandins [3]. Simultaneously, glucocorticoids stimulate gastric acid secretion [4,5].The mechanisms mediating the stimulatory effects on gastric acid secretion remained incompletely understood. On the one hand, glucocorticoids have been shown to enhance the degranulation of intramural mast cells with subsequently increased release of the secretagogue histamine [6].…”

Section: Introductionmentioning

confidence: 99%

PI3 Kinase Dependent Stimulation of Gastric Acid Secretion by Dexamethasone

Lang¹,

Schniepp²,

Kirchhoff³

et al. 2007

Cell Physiol Biochem

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Excessive gastric acid secretion plays an important role in the pathogenesis of peptic ulcers. Dexamethasone, a widely used drug, is known to stimulate gastric acid secretion and increase the incidence of peptic ulcers. However little is known about the mechanism of the dexamethasone’s effect on parietal cells. The present study was performed to investigate the contribution of the phosphatidylinositol-3-kinase (PI3 kinase) to dexamethasone induced stimulation of gastric acid secretion. In vivo pretreatment with dexamethasone injections (150µg/100g for 3 days) or in vitro exposure to (10 µM for > 20 minutes) significantly increased acid secretion in isolated gastric glands ñ 2-3 fold. The dexamethasone induced stimulation of gastric acid secretion was concentration dependent and significantly blunted by the H²⁺/K²⁺ ATPase inhibitor omeprazole (200 µM), the PI3 kinase inhibitor Wortmannin (500 nM), the protein kinase inhibitor staurosporine (2.5 µM) and the Cl^- channel blocker NPPB (100 µM); but not by the H₂ antagonist cimetidine (100 µM). In conclusion, it was observed that dexamethasone’s effect on proton extrusion requires the activity of a PI3 kinase pathway, an apical Cl^- channel and the H²⁺/K²⁺ ATPase.

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“…[Hirvonen, Kamppuri and Rasanen, 1967;Rasanen, 1969]. The mucosal mast cells differ from those occurring more deeply in the wall of the stomach in respect of various histochemical properties [Hakanson, Owman, Sjoberg and Sporrong, 1970;Heap and Kiernan, 1973], and can be selectively removed by treating the rat with dexamethasone for 3 days, a procedure which does not affect the mast cells elsewhere in the stomach or in the connective tissues of the skin [Rasanen, 1960[Rasanen, , 1964Haikonen and Rasanen, 1965;Heap and Kiernan, 1973]. Another drug, compound 48/80, degranulates and depletes all the mast cells in the body after 5 days of treatment with increasing doses [Riley, 1959].…”

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Mast Cells and Gastric Secretion in the Rat

Heap

Kibrnan

1975

Exp Physiol

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Gastric secretion of acid was measured in adult rats deprived of solid food for 48 hr. In control animals, values were obtained for the residual content of acid in the stomach, indicative of the rate of basal secretion, and for the quantities of acid secreted in 30 min following injections of histamine, pentagastrin, insulin and compound 48/80. The same measurements were made in groups of rats treated for 5 days with compound 48/80 (a regime which depleted the whole body of mast cells) and for 3 days with dexamethasone (which selectively depleted the gastric mucosa of mast cells). The content of residual acid was depressed to one third of the control value in the 48/80-treated rats, but the additional secretion due to histamine, pentagastrin or insulin was unaffected. A secretory response to a single injection of compound 48/80 could not be obtained in rats depleted of mast cells. In the dexamethasone-treated rats, the residual level of acid was increased to 1-5 times the control value, but the magnitudes of the responses to secretogogues were unchanged.It is concluded that basal secretion of acid into the stomach of the rat is stimulated by histamine derived from mast cells throughout the body, those of the gastric mucosa having no special significance in this respect. Mast cells are not involved in the mediation of the secretagogue actions of exogenous histamine, pentagastrin and insulin, but the present results do not preclude the participatiort of histamine from sources other than mast cells in the process of gastric secretion.The possible involvement of histamine in the secretion of acid by the gastric mucosa has been a controversial topic for many years. It has been suggested that stimulation of the oxyntic cells by histamine is a final common pathway for the secretagogue actions both of gastrin and of impulses carried in the parasympathetic nervous system [Code, 1965]. The evidence for such a function of the amine is strongest in the case of the rat [Grossman, 1967], where the rates of gastric mucosal formation [Kahlson, Rosengren, Svahn and Thunberg, 1964] and of urinary excretion [Lundell, 1974] of histamine are increased in states of heightened secretory activity. Moreover, burimimide, a drug which inhibits the secretion of acid in response to exogenous histamine, also blocks the response to gastrin [Black, Duncan, Durant, Ganellin and Parsons, 1972], and metiamide [Black, Duncan, Emmett, Ganellin, Hesselbo, Parsons and Wyllie, 1973], also blocks the response to vagal stimulation.Most of the histamine in the body is synthesized and stored in mast cells [Riley and West, 1953;Riley, 1959]. In the stomach, these cells occur abundantly in the connective tissue of the submucosal, muscular and serosal layers in all mammals [see Selye, 1965] and in the rat the cells are also numerous in the interglandular spaces of the mucosa [Rasanen, 1960;Foley and Glick, 1962;Heap and Kiernan, 1973]. It has been proposed that the mast cells of the mucosa are the source of the histamine which acts upon the oxyntic cells

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Hydrogen Ion Concentration in the Gastric Juice after Pylorus Ligation in Dexamethasone‐Treated Rat

Cited by 15 publications

References 13 publications

Histidine Induced Secretion in the Pyloric Ligated Rat Stomach

Histidine Induced Secretion in the Pyloric Ligated Rat Stomach

PI3 Kinase Dependent Stimulation of Gastric Acid Secretion by Dexamethasone

Mast Cells and Gastric Secretion in the Rat

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