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)

In 16 healthy subjects, gastric distention was produced by infusion of 5% mannitol solution, pH 5.5. Constant intragastric pressure was maintained by use of a barostat. Over successive 1-hr periods the head of pressure was raised in 5-cm increments from an arbitrary zero point to 15 cm. Gastric acid secretion was measured by constant intragastric titration. Blood samples were obtained throughout the study for measurement of serum gastrin concentrations. When intragastric pressure was raised from zero to 5 cm H2O, gastric acid secretion increased significantly (24% of peak acid response to pentagastrin). Acid responses at 10 and 15 cm pressure were lower. Serum gastrin concentrations increased slightly at 15 cm pressure but not at 5 or 10 cm. There was no correlation between increments in serum gastrin and acid secretory rates. We conclude that gastric distention at low pressures stimulated acid secretion by a mechanism and did not involve increases in circulating gastrin concentrations. Slight increases in serum gastrin observed at the highest distending pressure were not associated with further increases in acid secretion.
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PMID:Acid secretion and serum gastrin at graded intragasric pressures in man. 1 51

The effect of bilateral adrenalectomy and subsequent force-feeding of L-tryptophan on the gastric mucosal pepsin activity and [3H]leucine incorporation into total protein of the stomach (fundus) in vivo were investigated. One month after bilateral adrenalectomy the gastric mucosal pepsin activity and overall protein synthesis in the stomach were decreased by 72% and 52%, respectively. Twenty-four hours after a single tube-feeding of tryptophan (30 mg/100 g body weight) both activities returned to sham-operated control levels. In adrenalectomized rats the tryptophan-mediated stimulation of gastric mucosal pepsin activity was found to be sensitive to the RNA synthesis inhibitor, actinomycin-D. The diminution in gastric mucosal pepsin activity after adrenalectomy and its enhancement by tryptophan could not be related to the presence of an inhibitor or activator in the tissue. One month after adrenalectomy serum gastrin concentration was found to be 36% above that of the sham-operated control. In adrenalectomized rats, 24 and 48 h after tryptophan force-feeding, serum gastrin concentrations were decreased by 50% and 20%, respectively, but none of the values differed significantly from those of water-fed adrenalectomized controls.
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PMID:Bilateral adrenalectomy: effect of tryptophan on protein synthesis and pepsin activity in the stomach of rats. 11 8

The isolated, vagally innervated antral pouches in anesthetized dogs were irrigated with 095% acetylcholine chloride (Ach) or a 0.4 M mixture of non-essential amino acids (AA), or distended at 30 cm H2O pressure. In addition,2-deoxy-D-glucose (2-DG) was administered intravenously. Significant increases in antral venous gastrin, caused by gastrin releasers, were associated with a significant rise in cAMP content in the antral mucosa. Acidification of the antrum with simultaneous administration of 2-DG, and acidified AA abolished gastrin release, and significantly reduced mucosal cAMP. Acidified Ach and distension of the antrum with 0.1 N HC1 supressed gastrin levels without significantly changing the mucosal cAMP content. Since the augmented gastrin release was accompanied by an increased mucosal cAMP, the results suggest that cAMP participates in the action of gastrin secretagogues.
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PMID:Cyclic Amp and the release of antral gastrin. 19 27

In female rats aspirin-induced gastrin mucosal damage was increased and glycoprotein synthesis decreased by fasting and by insulin administration. Glucose added to the drinking water during the fasting period reduced mucosal damage and increased glycoprotein synthesis to control levels. Alloxan diabetes did not affect mucosal damage or glycoprotein synthesis. Alloxan diabetes plus insulin restored blood glucose levels to normal, and susceptibility to aspirin damage and glycoprotein synthesis were also normal. Alloxan diabetes plus fasting restored blood glucose levels to normal but increased aspirin-induced mucosal damage and reduced glycoprotein synthesis. In vitro incubation of gastric mucosal homogenates showed that diburyryl cyclic AMP and theophylline inhibited glycoprotein synthesis but dibutyryl cyclic GMP had no significant effects. The importance of an adequate supply of glucose to the gastric mucosa and the effects of cyclic nucleotides on glycoprotein synthesis are discussed.
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PMID:Effects of blood glucose levels on aspirin-induced gastric mucosal damage. 20 Jan 38

The previously described peptide material that reacts with antibodies to gastrin and is found in the central nervous system of various vertebrates is present in only the 100,000 X g pellet of postmortem human cerebral cortical grey matter. This immunoreactive material, extractable in boiling water, is biologically active on rat pancreatic preparations. On the basis of size, charge, immunological specificity, and patterns of biological activity, most of this material is closely related to the COOH-terminal octapeptide of cholecystokinin in its complete, sulfated biologically active form.
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PMID:Demonstration of biological activity of brain gastrin-like peptidic material in the human: its relationship with the COOH-terminal octapeptide of cholecystokinin. 27 70

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 chemistry, localisation, release and effects of gastrointestinal hormones and some related peptides are surveyed. Their main presumed physiologic actions are: gastric acid and pepsin secretion are stimulated by gastrin and to a less degree by secretin. Acid secretion is inhibited by bulbo-enterogastrone and GIP. Biliary water and electrolytes are augmented by gastrin, CCK-PZ, secretin and VIP and inhibited by Substance P. Pancreatic bicarbonate and enzyme secretions are stimulated by secretin and CCK-PZ, especially in combination. Lower oesophageal and antral motility and tonus are elevated following gastrin and motilin; the gallbladder and small intestine empty following CCK. Gastrin regulates gastrointestinal, and CCK pancreatic, tissue growth. Somatostatin inhibits all gut hormones. All peptides are vasoactive within the splanchnic area, each one in a specific manner.
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PMID:Gastrointestinal hormones. 35 98

The effect of the osmolarity of intragastric instillates on pepsin secretion was studied in rats anaesthetised with urethane. Irrigation of the stomach with solutions of sucrose and NaCl, resp. caused a concentration-dependent increase in pepsin output. A stimulation was observed already by hypotonic solutions and the maximal effect was obtained by 300 m-osmole/l of sucrose and by 600 m-osmole/l of NaCl (13- and 10-fold stimulation resp.). A similar time course in the increase of pepsin output was produced by hyperosmotic solutions (600 m-osmole/l) of sucrose, urea, NaCl and choline chloride. Pepsin output was stimulated maximally within 30 min and decreased thereafter, but remained at about 4--6-fold higher levels than during the previous irrigation with distilled water. Replacement of hyperosmotic instillates by distilled water reduced pepsin secretion to the initial level. Hypertonic ethanol (600 m-osmole/l) increased pepsin output only slightly. Vagotomy, pretreatment with atropine (1 mg/kg i.v.) or cimetidine (5 mg/kg i.v.), local anesthesia of the gastric mucosa with 4% lidocaine or intravenous infusion of PGE2 (2 microgram/kg X min) did not antagonise the stimulation of pepsin output induced by hyperosmotic NaCl (600 m-osmole/l). The results indicate that the increase of the osmolarity of intragastric instillates stimulates pepsin secretion in the rat without involvement of neural (vagal or local cholinergic reflexes) or hormonal mechanisms (release of gastrin) which are known to stimulate gastric secretion in the gastric phase.
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PMID:Osmotic stimulation of pepsin secretion in the rat. 35 99

The stomachs of six healthy volunteers were intubated with a Levine tube. In addition, a thin polyethylene tube was placed in the proximal jejunum or in the proximal duodenum. After a 1-h period with no perfusion the intestine was perfused for 2 h with 7% liver extract (LE) (pH 5.5; 380 MOsm/kg water) at a rate of 100 ml/h. In control tests 200 ml of 0.9% physiologic saline solution were used as perfusate. Reflux to the stomach was determined by addition of radioactive B12 to the perfusates. Plasma gastrin, gastric acid, and pepsin levels were measured in 15-min periods. During perfusion of the proximal jejunum only pepsin outputs were increased significantly. During duodenal perfusion of LE, gastric acid and pepsin outputs were increased to 31% and 73% of maximal pentagastrin stimulation, respectively. Controls showed no changes in gastric secretion. Plasma gastrin levels were not elevated after jejunal or duodenal perfusion. These results confirm that the intestinal phase of gastric secretory stimulation does exist in humans. Furthermore, it appears that the major portion of this stimulation originates from the duodenum and is not gastrin-dependent.
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PMID:Comparison of gastric secretory response in man to duodenal and jejunal liver extract perfusion. 38

Effect of intravenously administered bombesin has been studied on the in vivo and in vitro motor function of the lower esophageal sphincter (LES) of the opossum. Intraesophageal pressures were monitored by an assembly of polyvinyl catheters attached to pressure transducers and a recorder. The catheters were continuously perfused with bubble-free water. Intravenous administration of 5, 10, 30, 50, and 100 ng/kg bombesin stimulated the LES 4, 34, 106, 148, and 130%, respectively, above control values. Atropine and hexamethonium did not antagonize the response of the LES to bombesin. Tetrodotoxin, phentolamine, and reserpine all significantly antagonized the response of the LES to bombesin. The LES stimulatory effect of bombesin injected locally in the left gastric artery (LGA) was antagonized significantly by local administration of phentolamine in the LGA. Experiments performed in vitro (25 ml baths containing oxygenated Krebs solution) showed that bombesin (10(-9) M) increased the tone of LES strips, and the effect was antagonized by phentolamine (10(-6) M). Serum gastrin concentrations increased significantly only 15 min after bombesin administration. It is concluded that bombesin is a potent stimulant of the LES. The mechanism of stimulation involves a direct effect on the smooth muscle as well as an indirect one by an effect on the postganglionic adrenergic neurons releasing norepinephrine.
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PMID:Mechanism of lower esophageal sphincter stimulation by bombesin in the opossum. 43 39


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