Relation of gastric acid and pepsin secretion to serum gastrin levels in dogs given bombesin and gastrin-17

1983 ◽  
Vol 244 (5) ◽  
pp. G546-G551
Author(s):  
B. I. Hirschowitz ◽  
E. Molina
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Serum Gastrin ◽  
Gastric Fistula ◽  
Gastrin Release ◽  
Pepsin Secretion ◽  
Inhibitory Peptide ◽  
High Doses ◽  
Higher Doses ◽  
Stimulation Of

To quantitate bombesin stimulation of gastric acid and pepsin via release of gastrin, five gastric fistula dogs were given graded doses (60-1,250 pmol X kg-1 X h-1) of bombesin tetradecapeptide and 40-2,000 pmol X kg-1 X h-1 of synthetic gastrin-17 (G-17). Acid and pepsin output and serum gastrin were proportional to the dose of stimulant. The half-maximal dose of bombesin for gastrin release was 200 pmol X kg-1 X h-1. Bombesin-stimulated acid secretion related to serum gastrin concentrations was congruent with the G-17 curve, but with a maximum of only 62% of the G-17 maximum before declining by 27% despite higher serum gastrin levels. This suggested that bombesin stimulates acid secretion only via gastrin release and inhibits at higher doses by releasing another inhibitory peptide, most likely somatostatin, which is also released by bombesin. The same mechanism could apply to supramaximal inhibition of acid and pepsin seen with high doses of G-17. Because the pepsin curve related to serum gastrin was to the left of the G-17 curve, we concluded that another secretagogue released by bombesin acts synergistically with gastrin on pepsin secretion. Therefore, bombesin stimulates gastric secretion through gastrin release, but its effects are modified by peptides coreleased to a) increase pepsin output at low doses and b) limit the output of acid and pepsin to 50-60% of the G-17 maximum.

Gastric acid and pepsin hypersecretion in conscious rabbits

1991 ◽  
Vol 261 (2) ◽  
pp. G295-G304 ◽  
Author(s):  
J. S. Redfern ◽  
H. J. Lin ◽  
K. E. McArthur ◽  
M. D. Prince ◽  
M. Feldman
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Serum Gastrin ◽  
Gastric Fistula ◽  
Intragastric Ph ◽  
Pepsin Secretion ◽  
Cholinergic Pathways ◽  
Basal Serum ◽  
Maximal Output ◽  
Basal Acid

In conscious, gastric fistula rabbits, gastric acid and pepsin secretion averaged 4.5 +/- 0.1 mmol/h (1.3 mmol.kg-1.h-1) and 4.9 +/- 0.3 IU/h (1.6 IU.kg-1.h-1), respectively; these values represent approximately 40-50% of maximal output. Basal serum gastrin concentrations averaged 24 +/- 4 pg/ml and did not correlate with basal acid secretion. Atropine and vagotomy incompletely inhibited basal acid secretion (by 84 and 50%, respectively) and completely inhibited 2-deoxy-D-glucose-stimulated gastric acid secretion. Atropine and vagotomy similarly inhibited basal pepsin secretion by 50 and 40%, respectively. Ranitidine decreased acid and pepsin secretion, but as with atropine, inhibition was not complete (73 and 37%, respectively). Although omeprazole did not affect pepsin secretion, omeprazole completely inhibited basal acid secretion and elevated postprandial intragastric pH above 5.0. Conscious, gastric fistula rabbits have the highest basal acid and pepsin output among species commonly studied. Both vagal-cholinergic pathways and histamine drive basal acid and pepsin secretion in the rabbit.

Stimulation of gastric acid secreted by glycine and related oligopeptides in humans

1982 ◽  
Vol 242 (2) ◽  
pp. G85-G88
Author(s):  
A. Wald ◽  
S. A. Adibi
Keyword(s):  
Small Intestine ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Healthy Volunteers ◽  
Gastric Acid ◽  
Serum Gastrin ◽  
Physiological Saline ◽  
Glycine Concentration ◽  
Glycine Content ◽  
Stimulation Of

To investigate the effect of oligopeptides on gastric secretion in humans, we investigated acid secretion in healthy volunteers after the intragastric infusion of physiological saline, glycine (100 mM), diglycine (50 mM), triglycine (33 mM), and tetraglycine (25 mM). All test solutions were equivalent in glycine content, osmolality (300 mosmol), and pH (5.5). Although the rate of acid secretion was greater during glycine than saline infusion [5.6 +/- 0.8 vs. 3.3 +/- 1.1 mmol/h (means +/- SE); P less than 0.05], the rate of acid secretion during glycine infusion was not significantly different from that induced by its related peptides. There were increases in plasma glycine concentration during infusion of glycine and its related peptides but no detectable changes in serum gastrin levels. The increases in plasma glycine must have been due to absorption from the small intestine because there was no gastric absorption of glycine in free or dipeptide form nor diglycine hydrolysis in the stomach. Therefore, our results permit implicating only the increased plasma glycine concentrations as the stimulus for acid secretion by glycine and its homologous peptides.

scholarly journals Effects of antibodies to gastric inhibitory peptide on gastric acid secretion and gastrin release in the dog

1983 ◽  
Vol 84 (5) ◽  
pp. 941-948 ◽  
Author(s):  
M.Michael Wolfe ◽  
Michael P. Hocking ◽  
Daniel G. Maico ◽  
James E. McGuigan
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastrin Release ◽  
Inhibitory Peptide ◽  
Gastric Inhibitory Peptide

Effects of antral vagotomy in dogs on gastrin and gastric secretion with various stimuli

1990 ◽  
Vol 258 (6) ◽  
pp. G919-G925 ◽  
Author(s):  
B. I. Hirschowitz ◽  
J. Fong
Keyword(s):  
Gastric Secretion ◽  
Serum Gastrin ◽  
Vagal Stimulation ◽  
Gastric Fistula ◽  
Gastrin Release ◽  
Cholinergic Stimulation ◽  
Sham Feeding ◽  
Human Gastrin ◽  
Cholinergic Effects ◽  
Stimulation Of

In four gastric-fistula dogs, selective antral vagotomy markedly reduced the vagal stimulation of gastrin release, thereby defining both the vagal pathway for stimulation of gastrin and the anatomic source of such gastrin release. Despite loss of gastrin response, vagal excitation by 100 mg/kg 2-deoxy-D-glucose (2-DG) produced the same acid and pepsin responses after antral vagotomy as before, but there was an approximately 40% diminished fundic response to pentagastrin, histamine, and synthetic human gastrin, as well as to endogenous gastrin released by graded doses of bombesin. Bethanechol did not reverse the defect, ruling out inadvertent fundic vagal denervation, nor did raising serum gastrin by bombesin alter the response to vagal stimulation by 2-DG. Fundic response to bethanechol was increased by approximately 60%, and the output of gastrin increased at least fivefold after antral vagotomy. Gastrin responses to food were diminished and those to sham feeding were eliminated. Separation of the denervated antral pouch had no additional effect on acid secretion. Vagal stimulation of gastric secretion thus occurs almost exclusively through direct cholinergic effects on the fundus with little or no contribution from antral gastrin. Vagal denervation sensitizes the antrum to cholinergic stimulation.

Intracisternal injection of a TRH analogue stimulates gastric luminal serotonin release in rats

1989 ◽  
Vol 256 (2) ◽  
pp. G377-G383 ◽  
Author(s):  
R. L. Stephens ◽  
Y. Tache
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Receptor Activation ◽  
Gastric Fluid ◽  
Serotonin Release ◽  
Gastric Fistula ◽  
Intracisternal Injection ◽  
Gastric Lumen ◽  
Stimulation Of

Intracisternal injection of TRH analogue, RX 77368, which has been previously shown to induce a vagal-dependent stimulation of gastric acid secretion and contractility dose-dependently (10-300 ng) stimulated serotonin release into the gastric lumen of conscious pylorus-ligated rats. The stimulation of gastric acid and serotonin release occurred 15 and 30 min, respectively, after intracisternal injection of RX 77368 (100 ng) and lasted for over 2 h, as measured in urethan-anesthetized rats with gastric fistula. Cervical vagotomy and atropine pretreatment (0.1 mg/kg) completely abolished the RX 77368-stimulated gastric serotonin and acid output in acute gastric fistula rats, whereas in pylorus-ligated rats atropine pretreatment markedly reduced RX 77368-stimulated gastric fluid volume and serotonin output, but not serotonin concentration. Systemic administration of bethanechol chloride, histamine, or pentagastrin, at doses that elicited gastric acid secretory responses similar to that of intracisternal TRH analogue, produced little or no intraluminal serotonin release. These results demonstrate that intracisternal injection of TRH analogue induced a marked and sustained release of serotonin into the gastric lumen that is mediated by vagal-dependent mechanisms unrelated to enhanced acid secretion. Activation of muscarinic receptors appears to be involved, but the relative ineffectiveness of bethanechol in this system suggests that (an)other vagally mediated neurochemical event(s) stimulated by intracisternal RX 77368 acts in conjunction with muscarinic receptor activation to produce intraluminal serotonin release. The functional significance of serotonin release into the gastric lumen in relation with intracisternal TRH analogue-induced alterations of gastric secretion, motility and blood flow, and lesion formation remains to be elucidated.

Inhibition of bombesin-stimulated acid secretion by immunoneutralization of gastrin in dogs

1995 ◽  
Vol 268 (1) ◽  
pp. G54-G58
Author(s):  
T. O. Kovacs ◽  
K. C. Lloyd ◽  
H. Wong ◽  
J. H. Walsh
Keyword(s):  
Monoclonal Antibody ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Fistula ◽  
Gastrin Release ◽  
Gastric Acid Output ◽  
Plasma Gastrin

Bombesin-like peptides stimulate gastrin release and gastric acid secretion. The increase in gastric acid output is thought to be secondary to gastrin release. A monoclonal antibody (MAb) directed specifically to gastrin (MAb 28.2) was used to study the role of circulating gastrin in the regulation of bombesin-stimulated acid secretion in dogs. Seven conscious, fasted dogs with gastric fistulas received intravenous bombesin infusions in fourfold increasing doses from 200 to 3,200 pmol.kg-1.h-1. Each dose was given for 45 min. On separate days, dogs were pretreated with an intravenous infusion of 7 mg of MAb 28.2 or vehicle (0.1% canine serum albumin). Samples of gastric effluent were collected by gravity drainage through the gastric fistula, and acid output was measured by titration of gastric effluent to pH 7.0, using 0.2 N NaOH. Plasma gastrin concentrations were determined by radioimmunoassay. Bombesin infusion produced dose-dependent increases in plasma gastrin concentrations and gastric acid output. Administration of gastrin MAb 28.2 abolished bombesin-stimulated gastric acid output. Immunoneutralization of circulating gastrin in vivo using a gastrin monoclonal antibody in dogs indicates that the acid stimulatory response to bombesin is mediated by gastrin.

Evidence for reflex adrenergic inhibition of acid secretion in the conscious rat

1986 ◽  
Vol 251 (5) ◽  
pp. G615-G618 ◽  
Author(s):  
R. Dimaline ◽  
N. Carter ◽  
S. Barnes
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Chemical Stimulation ◽  
Gastric Distension ◽  
Gastric Fistula ◽  
Conscious Rat ◽  
Basal Acid ◽  
Stimulation Of

In conscious gastric fistula rats, gastric distension with saline to a pressure of 7 cm caused a threefold reduction of basal gastric acid secretion. Distension with 6.25% peptone solution to the same pressure doubled basal acid secretion. The saline distension-induced inhibition was abolished by guanethidine and markedly reduced by propranolol; phentolamine was ineffective. The response to peptone was unaffected by guanethidine. The results suggest that in the rat, gastric distension at physiological pressures inhibits acid secretion by a beta-adrenergic reflex. The inhibition can be masked by concurrent chemical stimulation of the gastric mucosa by the digestion products of food.

Effects of tachykinins on gastric acid and pepsin secretion and on gastric outflow in the Atlantic cod, Gadus morhua

1986 ◽  
Vol 250 (3) ◽  
pp. G309-G315 ◽  
Author(s):  
B. Holstein ◽  
C. Cederberg
Keyword(s):  
Substance P ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Gastric Volume ◽  
Pepsin Secretion ◽  
Secretory Rate ◽  
Related Peptide ◽  
High Doses

Gastric acid and pepsin responses to substance P, physalaemin, eledoisin, and an eledoisin-related peptide, [Lys6]eledoisin-(6-11), were measured in gastrically and intestinally perfused cods. The intestinal perfusion maintains water balance and inhibits drinking. During basal conditions acid secretion was stimulated (approximately equal to 25%) by low doses (less than 0.13 nmol X kg-1 X h-1) of physalaemin and eledoisin. High doses (greater than 16 nmol X kg-1 X h-1) were inhibitory. Median and very high doses of substance P and eledoisin-related peptide, respectively, tended to stimulate acid secretion. All tachykinins were extremely efficacious pepsigogues. Physalaemin and eledoisin were the most potent (D50 approximately 10(-10) mol X kg-1 X h-1) but produced fading and submaximal responses at high doses. The fading persisted despite endogenous acidification produced by histamine stimulation. Relative to physalaemin, the potencies of substance P and eledoisin-related peptide were 0.04 and 0.001. The results suggest that some tachykinin may be a physiological stimulator of pepsin secretion and that the effect on acid secretion results from activation of both stimulatory and inhibitory pathways. The inhibitory component probably includes a cholinergic link. Gastric volume outflow increased during infusion of physalaemin, eledoisin, and (slightly) substance P. The response, which was not related to acid secretory rate (and conceivably not to volume secretion), suggests that a tachykinin may be involved also in the regulation of drinking.

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