Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Secretion of HCl and pepsin from abomasal fundic pouches was studied in sheep during perfusion of antral pouches with cholinergic blocking and stimulating agents and lignocaine. 2. Resting secretion was reduced to about 50% of control levels and secretory responses to feeding were largely or completely blocked during antral pouch perfusions with atropine (0-01-0-16%) and hexamethonium (1%). 3. Antral pouch perfusions with lignocaine (2%) reduced fundic pouch resting secretion to about 60% of control values but did not block secretory responses to feeding. 4. Perfusions of acetylcholine (0-1%) and carbachol (0-0037 and 0-005%) through antral pouches characteristically stimulated increases in the concentration of acid, outputs of acid and pepsin, but not concentration of pepsin. 5. The mechanisms involved in the release of gastrin in the sheep are discussed. 6. It is concluded that antral secretion of gastrin contributes both to the maintenance of resting secretion of acid and the secretory responses of fundic pouches of sheep when they eat freshly provided food.
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PMID:Acid and pepsin secretion of separated gastric pouches during perfusion of antral pouches with cholinergic stimulating and blocking agents and lignocaine. 32 Mar 8

1. In dogs with gastric fistulas and vagally innervated fundic and antral pouches, 13-norleucine-motilin (13-nle-motilin), a synthetic analogue of motilin, infused intravenously in graded doses produced a dose-dependent increase in gastric acid and pepsin outputs. 2. The motilin-induced stimulation of gastric secretion occurred independently of antral pH and was not accompanied by any alteration in the serum gastrin level suggesting that motilin did not affect the release of gastrin. 3. When infused intravenously in a constant dose against a constant background stimulation with pentagastrin or histamine 13-nle-motilin inhibited both acid and pepsin secretion from the main stomach and fundic pouch. 4. The inhibitory effect of 13-nle-motilin was always associated with a marked reduction in mucosal blood flow but without any change in the ratio of aminopyrine concentration in the gastric juice and blood plasma indicating that this peptide primarily affected gastric secretion but did not limit the gastric mucosal microcirculation.
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PMID:Effect of 13-NLE-motilin on gastric secretion, serum gastrin level and mucosal blood flow in dogs. 32 55

We have studied the gastric response to an ordinary solid-liquid meal in 12 patients with active duodenal ulcer and 8 healthy volunteers. Our method employs gastric and duodenal markers to quantify acid, pepsin, and volume outputs in response to the meal, without manipulating intragastric pH. Intragastric volume, rate of gastric emptying, delivery of acid into the duodenum, and serum gastrin response were also measured simultaneously. On a separate day, peak acid output in response to betazole (1.5 mg per kg subcutaneously) was determined. Our results indicate an inappropriately prolonged gastric secretory response to meals in duodenal ulcer disease, without a concomitant increase in peak postprandial secretory rates or an increase in serum immunoreactive gastrin levels. Further, the stomach in duodenal ulcer disease did not "retain" the additional acid secreted in the later postprandial period, and abnormally high rates of acid delivery into the duodenum occurred. Our data are consistent with a dual defect in the duodenal mechanisms regulating both acid secretion and acid delivery into the duodenum.
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PMID:Gastric secretion and emptying after ordinary meals in duodenal ulcer. 33 82

A case with proteinlosing gastropathy with gastric hypersecretion of H+ and pepsin as well as hypergastrinemia is presented. Zollinger-Ellison syndrome was excluded by reduction in acid secretion and serum gastrin during the observation period as well as by the effect on gastric secretion and serum gastrin after injections of secretin and glucagon.
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PMID:Proteinlosing gastropathy with gastric hypersecretion of acid (H+) and pepsin and hypergastrinemia. A case report. 33 48

The effect of threshold dose of methacholine on gastric secretion stimulated by pentagastrin (PG) was studied in two groups of cats, four with Pavlov pouches (PP) and four with Heidenhain pouches (HP). In the PP group methacholine did not alter the maximal response (MR) and the dose producing half of the maximal response (D50) for PG. In the HP group the highest acid response to PG combined with methacholine was greater than the MR to PG alone. Methacholine decreased the D50 for PG in the HP group to that in the PP group with and without methacholine. Methacholine increased the pepsin response to all doses of PG both in the PP and the HP groups. The effect was more pronounced in the HP group. In both types of pouches, the percentage increase of pepsin secretion was larger at low than at high doses of PG. Methacholine increased the pepsin/acid (P/A) ratio for PG in the HP group to that in the PP group with and without methacholine. Accordingly, methacholine sensitized the oxyntic glands and increased the pepsin response to PG in the HP group as did basal vagal tone in the PP group. Methacholine did not further sensitize the innervated oxyntic glands to gastrin but increased the response of the peptic glands.
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PMID:Effect of methacholine on acid and pepsin responses to pentagastrin in cats with innervated and denervated fundic pouches. 33 50

The effect of somatostatin, a growth hormone releasing-inhibiting hormone (GH-RIH) on basal and meal-, pentagastrin-, or histamine-stimulated gastric acid and pepsin secretion was studied in six duodenal ulcer patients. Intravenous GH-RIH infused in graded doses ranging from 0.62 to 5.0 microgram/kg/hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 15% of control level at the dose of 5.0 microgram/kg/hr. Acid inhibition was paralleled by a decrease in the pepsin output and accompanied by a dose-dependent reduction in serum growth hormone and insulin levels measured by radioimmunoassay. GH-RIH used in a single dose of 2.5 microgram/kg/hr produced about 85% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in serum gastrin and insulin levels. The effect of GH-RIH on histamine-stimulated secretion was very modest and observed only after stopping the GH-RIH infusion. Thus GH-RIH suppressed acid and pepsin secretion induced by pentagastrin and a meal, and this effect was accompanied by a suppression of serum growth hormone and gastrin levels which may contribute to the inhibition of gastric secretion observed.
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PMID:Effect of somatostatin on meal-induced gastric secretion in duodenal ulcer patients. 33 84

In rats under either mild stress (= controls) or severe stress (= restraint) gastric secretion (acid; pepsin, volume), mucosal blood flow, serum gastrin and ulcer formation were evaluated without and with additional infusion of a low dose (0.25 mg/kg.h) metiamide over an 8 h experimental period. Calculated constants of dose-response characteristics for acid output in this species are: Km = 1.41 +/- 0.36 mg/kg.h; Vmax = 94.4 +/- 11.0 per cent. Restraint depresses markedly secretion and microcirculation, but stimulates ulcer formation and raises serum gastrin. In controls, metiamide inhibits secretion and ulcer index significantly, but leaves mucosal blood flow and gastrin unaltered. In contrast, with restraint and metiamide, ulcer index was not improved, whereas mucosal blood flow was restored to almost control levels. Therefore, H2-receptor blockers, in addition to inhibition of secretion, may interfere with microcirculation either directly or by secondary release of yet unknown mediator substance(s), depending on the prevailing tissue environment.
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PMID:Rat gastric secretion and mucosal blood flow during restraint stress--effect of a low dose metiamide. 33 7

Three experiments were carried out in each of 6 healthy students on separate days, in a randomized order. Intravenous saline infusions were given for one hour basally in each experiment. During the second hour either pentagastrin, pentagastrin and somatostatin, or somatostatin alone were given. Gastric juice was collected continuously during all experiments. Somatostatin decreased the volume of gastric secretion and the concentrations of acid and pepsin, and output of acid, pepsin, and intrinsic factor (IF). The plasma gastrin concentration was not changed by somatostatin. A rebound effect was seen on pepsin and IF outputs after cessation of somatostatin, and on blood sugar concentration. The present study suggests that somatostatin acts on gastric secretion either directly or by mechanisms other than by inhibition of gastrin. The rebound of pepsin and IF indicates a release-inhibiting action on these substances similar to the effect of somatostatin on the release of some hormones.
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PMID:The effect of somatostatin on pentagastrin-stimulated gastric secretion and on plasma gastrin in man. 33 22

The stomachs of 8 healthy volunteers were intubated with a Levine tube under radiological control. In addition, a thin polyethylene tube was placed in the proximal duodenum. After a 1-hour period with no perfusion, the duodenum was perfused for two hours with 15% liver extract (LE) (pH 4.5--5.5; 1027 mosm/kg water) at a rate of 100 ml/hour either alone or in combination with intravenous infusion of different doses of exogenous pentagastrin. All subjects were also tested with the tubes in place for 3 hours, but with no perfusion or pentagastrin. Reflux to the stomach was monitored by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin were measured in 15-minute periods. During perfusion of the proximal duodenum, where reflux of the perfusates was less than 4%, only a slight and inconstant change in plasma gastrin was seen. Gastric acid and pepsin outputs were increased to approx. 18% and 25% of the maximal pentagastrin stimulation respectively. Whereas 15% LE was shown to release gastrin by antral perfusion however, such release was not found by duodenal perfusion, except where reflux to the antrum was seen. The results suggest that intestinal stimulation of gastric secretion exists, but has not been found to be gastrin dependent in the present investigation.
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PMID:Plasma gastrin and gastric secretory response to duodenal perfusion with liver extract in healthy human subjects. 33 24

The stimulating effect of AOC-tetragastrin, caerulein, Histalog and secretin on human gastric acid and pepsin secretion was studied in gastric ulcer patients. The pattern of gastric acid and pepsin secretion after the administration of caerulein was closely resembled to that of gastrin. Slight increase of pepsin secretion after gastrin or caerulein could be based on "wash-out" action caused by the increase of acid secretion after the stimulants. Stimulating effect on gastric pepsin secretion of histalog and secretin would be independent of gastric acid secretion.
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PMID:Clinical study on gastric secretion with special reference to pepsin secretion. 34 50


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