Inhibitory effect of ouabain on in vitro and in vivo gastric acid secretion in the frog and the rat

1984 ◽  
Vol 40 (8) ◽  
pp. 809-812
Author(s):  
E. S. K. Assem ◽  
B. Y. C. Wan
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Effect

Radioreceptor and biological characterization of cholecystokinin and gastrin in the chicken

1984 ◽  
Vol 246 (3) ◽  
pp. G296-G304
Author(s):  
S. R. Vigna
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Amylase Secretion ◽  
Physiological Regulation ◽  
Chicken Brain ◽  
Specific Radioimmunoassay ◽  
Cck Receptor Antagonist

Radioimmunoassay, radioreceptor assays, and bioassays were used to demonstrate that chicken brain and antrum extracts contain cholecystokinin (CCK)-like and gastrinlike peptides, respectively. C-terminal-specific radioimmunoassay of partially purified chicken CCK and gastrin gave dilution curves parallel to those of the mammalian peptides. Mouse cerebral cortical and rat pancreatic membrane radioreceptor assays were used to differentiate CCK- from gastrinlike peptides on the basis of the different CCK versus gastrin specificities of the two receptors. Confirmation of the biological activity of chicken brain CCK was obtained by stimulation of amylase secretion from rat pancreatic lobules in vitro. The specificity of this response was demonstrated by the inhibition of chicken CCK-stimulated amylase secretion by the specific CCK receptor antagonist dibutyryl cGMP. Chicken antral gastrin stimulated gastric acid secretion from the rat stomach in vivo. In contrast to previous hypotheses, it is proposed that chickens have significant amounts of an antral gastrinlike peptide and that therefore it is possible that gastrin is involved in the physiological regulation of gastric acid secretion in chickens.

Relationship between maternal milk PGE2 and gastric acid secretion in newborn rats

1990 ◽  
Vol 259 (5) ◽  
pp. G702-G708
Author(s):  
A. Wirbel ◽  
R. Ducroc ◽  
B. Garzon ◽  
C. Merlet-Benichou ◽  
J. P. Geloso
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Sesame Oil ◽  
Newborn Rats ◽  
Maternal Milk ◽  
Infant Rats

We previously demonstrated that in rats gastric acid secretion declines after birth and drops steeply on day 12 of life. In the present study, we investigated the part played in this decline by prostaglandin E2 (PGE2) from maternal milk. PGE2 content was first measured in the milk of untreated dams 0, 1, 5, 10, 12, 15, and 18 days after parturition. PGE2 levels were high during the first 5 days (123.5-200.5 pg/ml), declined significantly between days 10 and 15 (56.6-85.4 pg/ml; P less than 0.05), and dropped to 18.4 pg/ml on day 18. We also found that depleting milk of PGE2 prevented drop of acid secretion in 12-day-old suckling rats. Injecting lactating dams with indomethacin significantly reduced milk PGE2 content by 65% vs. milk of untreated dams. Surprisingly, administration of sesame oil, the indomethacin vehicle to the dams, increased milk PGE2 content by 182%. In the pups of the indomethacin-treated dams, acid secretion did not drop. On the contrary, in vivo basal and histamine-induced acid output rose markedly by 40 and 50%, respectively, and in vitro the net movements of 36Cl and 22Na measured in the isolated stomach indicated that active Cl- secretion had resumed. Mucosal PGE2 did not appear to be significantly involved in early development of acid secretion because administration of indomethacin to pups from untreated dams did not significantly modify the secretion measured on day 12. Data indicate that maternal milk depletion of PGE2 prevents the drop of gastric acid secretion previously observed in 12-day-old pups and suggest that in infant rats maternal PGE2 plays a physiological part in regulating acid secretion.

Measurement of meal-stimulated gastric acid secretion by in vivo gastric autotitration

2002 ◽  
Vol 92 (2) ◽  
pp. 427-434 ◽  
Author(s):  
Jerry D. Gardner ◽  
Arthur A. Ciociola ◽  
Malcolm Robinson
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Solid Meal ◽  
Standard Meal ◽  
Specialized Equipment ◽  
Reproducible Method ◽  
Time Required

Measurement of meal- stimulated gastric acid secretion using manual intragastric titration is demanding in terms of personnel and specialized equipment. In the present study, we used a new method, in vivo gastric autotitration, to determine meal-stimulated gastric acid secretion. Gastric pH was measured every 4 s before, during, and after ingestion of a standard meal in 24 healthy subjects. Placebo, ranitidine (150 mg), ranitidine (75 mg), or famotidine (10 mg) was given 1 h after the beginning of the meal. Meal-stimulated gastric acid secretion was calculated from the amount of HCl required to titrate the homogenized standard meal to pH 2 in vitro (119 mmol) and the time required for the pH of the ingested meal to decrease to pH 2 in vivo. Values for pH were also converted to acid concentration (mM), and integrated acidity was calculated from the cumulative, time-weighted means of the acid concentrations for every fourth second of the postprandial recording period. Control meal-stimulated gastric acid secretion was 60 (40–71) mmol/h (median; interquartile range), and each histamine H2-receptor antagonist significantly decreased secretion by ∼50%. Meal-stimulated acid secretion correlated directly with postprandial integrated gastric acidity ( r = 0.72; P = 0.0001). Thus intragastric autotitration is a convenient, reproducible method for measuring gastric acid secretion after ingestion of a solid meal and offers several advantages over manual intragastric titration.

Inhibition of the alpha-amidation of gastrin: effects on gastric acid secretion

1990 ◽  
Vol 258 (5) ◽  
pp. G810-G814 ◽  
Author(s):  
C. J. Dickinson ◽  
L. Marino ◽  
T. Yamada
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Enzyme Synthesis ◽  
Normal Serum ◽  
Biologically Active ◽  
Sprague Dawley

Formation of biologically active amidated gastrin from glycine-extended progastrin processing intermediates (G-Gly) is achieved via the action of peptidyl-glycyl alpha-amidating monooxygenase. Since this enzyme requires copper for optimal activity, we examined the effects of a known copper chelator, diethyldithiocarbamate (DDC), on gastrin posttranslational processing and gastric acid secretion in vivo. DDC (400 mg.kg-1.day-1 ip X 3 days) administered to male Sprague-Dawley rats decreased antral amidated gastrin content, but increased antral G-Gly content. The ratio of amidated gastrin to G-Gly, which reflects in situ amidating activity, was decreased in DDC-treated rats. In contrast, tissue amidating potential, assayed directly under optimal copper concentrations in vitro, was increased in the antrum and unchanged in the pituitary. DDC markedly increased both basal and gastrin-stimulated gastric acid outputs despite the presence of normal serum amidated gastrin levels. These results suggest that copper chelation with DDC inhibits amidating activity in situ but selectively increases antral amidating enzyme synthesis. The marked increase in acid secretion despite normal circulating amidated gastrin concentrations, combined with the enhanced secretory response to exogenously administered gastrin, suggests the possibility that gastrin receptors are upregulated by the events precipitated via DDC administration.

Effects of verapamil on gastric acid secretion in vitro and in vivo

1988 ◽  
Vol 156 (3) ◽  
pp. 341-350 ◽  
Author(s):  
Andreas W. Herling ◽  
Magnus Ljungström
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid

Inhibition of gastric H+ secretion, K+-ATPase and K+-phosphatase by estradiol in vivo and in vitro

1982 ◽  
Vol 60 (5) ◽  
pp. 680-684 ◽  
Author(s):  
L. Limlomwongse ◽  
P. Piyachaturawat
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Enzyme Activities ◽  
Direct Action ◽  
Inhibitory Effect ◽  
Secretory Rate ◽  
Dose Dependent

The effect of estrogen on the gastric acid secretion and H+-transporting enzymes, K+ -ATPase and K+-phosphatase, were investigated in the rat. The maximum H+ secretory rate in response to 1 mM histamine was significantly reduced (P < 0.05) in both the isolated gastric mucosa obtained from the rats treated with estradiol in vivo for 7 days and the mucosa directly incubated in vitro with estradiol. The inhibitory effect on the gastric enzyme activities in vitro showed a dose-dependent pattern of a noncompetitive type. The result suggested that estradiol may have a direct action on the gastric H+ secretion by inhibiting the H+ transport enzyme activities.

Effects of Cannabinoid Receptor Agonists on Rat Gastric Acid Secretion: Discrepancy Between In Vitro and In Vivo Data

2006 ◽  
Vol 51 (2) ◽  
pp. 310-317 ◽  
Author(s):  
Gabriella Coruzzi ◽  
Maristella Adami ◽  
Elena Guaita ◽  
Alessandro Menozzi ◽  
Simone Bertini ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Cannabinoid Receptor ◽  
Receptor Agonists

Immunoneutralization of somatostatin and neurotensin: effect on gastric acid secretion

1988 ◽  
Vol 255 (1) ◽  
pp. G40-G45 ◽  
Author(s):  
A. Seal ◽  
E. Liu ◽  
A. Buchan ◽  
J. Brown
Keyword(s):  
Monoclonal Antibodies ◽  
Small Bowel ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Cell Lines ◽  
Inhibitory Effect ◽  
Gastric Fistula ◽  
Distal Small Bowel

Cell lines producing monoclonal antibodies to somatostatin and neurotensin, designated S-10 and NT-C5, respectively, have recently been generated. The purpose of the present immunoneutralization study in urethan-anesthetized gastric fistula rats is 1) to examine the ability of these antibodies to block the inhibitory effect of their target peptides on meal-stimulated gastric acid secretion and 2) to use these antibodies as probes to determine whether somatostatin and/or neurotensin are involved in the inhibition of gastric acid secretion produced by intraduodenal, intra-ileal, and intracolonic fat infusions. The results demonstrate that both S-10 and NT-C5 successfully bound exogenous somatostatin and neurotensin in vivo. S-10 but not NT-C5 prevented the inhibition of gastric acid secretion produced by intraduodenal fat. NT-C5 but not S-10 prevented the inhibition of gastric acid secretion produced by intra-ileal fat. Neither S-10 nor NT-C5 prevented the inhibition of gastric acid secretion produced by intracolonic fat. We conclude that somatostatin is associated with proximal and neurotensin with distal small bowel intestinal fat-induced inhibition of gastric acid secretion.

Tonic suppression of gastric acid secretion by endogenous peptides in neonatal rats

1995 ◽  
Vol 269 (5) ◽  
pp. G721-G728
Author(s):  
R. K. Rao ◽  
S. Pepperl ◽  
F. Porreca
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Neonatal Rats ◽  
In Vitro Techniques ◽  
Basal Acid ◽  
Old Rats

Stimulation of gastric acid secretion by secretagogues was measured in developing rats by in vivo and in vitro techniques. Basal acid outputs in vivo were very low in 8- and 14-day-old rats compared with those in 20- and 30-day-old rats. In 20-day-old rats, all secretagogues increased acid output in vivo, whereas only carbachol, pentagastrin, and sulfated cholecystokinin octapeptide (CCK-8S) were active in 14-day-old rats. In contrast, basal acid output in vitro and stimulation by secretagogues did not differ significantly with age. CCK-8S-stimulated acid output in vitro in 14-day-old rats was blocked by L-365,260, L-364,718, tetrodotoxin, and atropine, but not by hexamethonium, whereas gastrin-stimulated acid output was blocked only by L-365,260. Furthermore, acid output in vivo was elevated three- to fourfold by subcutaneous naloxone-methiodide or L-364,718, but not by L-365,260, in 14-day-old rats; none of these antagonists produced an effect in 20-day-old rats. These studies show that low basal gastric acid output in neonatal rats is caused by tonic inhibitory regulation by endogenous regulatory peptides.

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