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)

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 aim of this work was to further investigate whether it is possible, through parietal cell vagotomy (PCV), to obtain both a complete suppression of the gastric secretory response to vagal impulses and to retain a normal contractile response of the antral muscle. Acid and peptic secretions, the electrical activity and the force of circular antral contractions were simultaneously studied in dogs, before and after PCV, under 2-deoxy-D-glucose (2DG) and pentagastrin (PG) stimulation. After PCV, the response to 200 mg/kg 2DG was reduced by about 70% for acid and 80% for pepsin; the slopes of the dose-response curves were significantly reduced after PCV. The slope of the regression line pepsin/acid after 2DG was decreased following PCV. The mean acid response to PG was reduced about 50% after PCV. Plasma immunoreactive gastrin increased following 2DG, and the variations were identical before and after PCV. The gastric control electrical activity in basal conditions (fasted dogs) and following 2DG was similar before and after PCV. The antral contractile response to 2DG was reduced by about 40% after PCV. In conclusion, when PCV induced an 80% reduction in the gastric secretory response to maximal vagal stimulation by 2DG, the contractile antral response was not entirely normal. This effect might be due either to a partial antral denervation or to some intrinsic influence of the denervated gastric body upon the strength of antral contractions.
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PMID:Parietal cell vagotomy in dogs. A comparative study of the effects on gastric secretion and antral muscle contraction. 36 72

The ability of an amino acid mixture given intraduodenally or intravenously to stimulate gastric secretion is compared in healthy subjects and in duodenal ulcer patients. Graded amounts of amino acids by both routes produced a similar increase in acid output in healthy subjects, reaching about 30% of the maximal response to pentagastrin. Serum gastrin concentrations remained virtually unchanged but serum alpha amino acid nitrogen levels were about twice as high with intravenous as with intraduodenal administration. Intravenously administered amino acids produced a significantly higher acid output in patients with duodenal ulcer than in healthy subjects, but did not produce a significant increase in gastric acid or pepsin secretion when combined with a pentagastrin infusion as compared with pentagastrin alone. Cimetidine (2 mg/kg/h) added to intravenous amino acid infusions caused almost complete suppression of acid secretion. This study indicates that amino acids are capable of stimulating gastric secretion after intraduodenal and after intravenous administration. The response to the latter is significantly higher in patients with duodenal ulcer than in healthy subjects, does not appear to involve gastrin release, is not affected by pentagastrin, and is strongly suppressed by histamine H2-blocker.
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PMID:Comparison of intraduodenal and intravenous administration of amino acids on gastric secretion in healthy subjects and patients with duodenal ulcer. 36 9

This paper presents evidence for the existence in extracts from porcine non-antral gastric tissue of a peptide capable of causing substantial rises of plasma immunoreactive gastrin levels in a dose dependent manner and of stimulation of gastric acid and pepsin secretion. Obtained data show that the peptide is basic and that its gastrin releasing properties are at least partially resistant to atropinisation and beta-receptor blockade. Antrectomy almost eliminates the rise in plasma IRGa when the peptide is administered. The possible relationship of this peptide to amphibian bombesin is discussed.
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PMID:A gastrin releasing peptide from the porcine nonantral gastric tissue. 36 11

Bovine pancreatic polypeptide was infused intravenously in 16 healthy volunteers at a mean dose of 218 pmol/kg/hr, producing plasma levels similar to those after meals. Basal and pentagastrin-stimulated acid and pepsin outputs and plasma gastrin concentrations were unchanged by BPP. Pancreatic polypeptide is unlikely to be an important physiological modulator of these secretions in man.
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PMID:Effect of bovine pancreatic polypeptide on gastric acid and pepsin output in man. 36 11

1 Daily ethinyloestradiol (50 mug) and norethisterone acetate (1 mg) treatment (Minovlar) was investigated on gastric acid and pepsin secretion, and fasting serum gastrin concentration in six conscious female cats prepared with chronic gastric fistulae. The effect on biliary secretion of bile acids, phospholipids, and cholesterol was investigated in three conscious female cats prepared with chronic gastric and intestinal fistulae, and cholecystectomy.2 Treatment for 49 days did not alter the gastric acid or pepsin response to either intravenous pentagastrin infusions or a food stimulus. The fasting serum gastrin concentration remained unaltered throughout the study.3 Treatment for 18 days did not alter the percentage concentration of cholesterol in the bile, but reduced the percentage concentration of phospholipid. This was mirrored by a rise in the percentage concentration of bile acids in the bile. These trends were quickly reversed on cessation of treatment.4 There was no sign of cholestasis associated with the treatment. Intestinal flow remained constant throughout the study, there was no lithocholic acid or other abnormal bile acids detectable in any samples, and there was no change in serum aspartate aminotransferase concentration.5 The results suggest that in female cats, treatment with a combined oestrogen-progestin preparation does not exert any beneficial effects on the aetiology of peptic ulceration through the reduction of acid or pepsin secretion, or the lowering of serum gastrin concentration. The preparation shows a tendency to produce more lithogenic bile, and this may partly explain the greater incidence of gall stones in women on the contraceptive pill.
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PMID:Effects of a combined oestrogen-progestin preparation on gastric acid and pepsin secretion, serum gastrin concentration and biliary secretion of bile acids, phospholipids, and cholesterol in the cat. 36 77

The histamine H-2 receptor antagonist cimetidine was given for 90 minutes to four fistula dogs during a steady dose 270-minute infusion of histamine (50 microgram. base/kg.hr.), urecholine (80 microgram./kg.hr.) or pentagastrin (1.5 microgram./kg.hr). In each case there was gradual but marked (75-95%) inhibition of acid secretion with maximal effects after 60-90 minutes while pepsin secretion was also suppressed but to a lesser extent. These effects persisted for at least the 90 minutes after the end of cimetidine infusion. Serum gastrin was not significantly changed by cimetidine. Kinetics of effect of cimetidine were derived from stepdose responses to histamine (2-150 microgram./kg.hr.), pentagastrin (0.1 to 10 microgram.kg.hr.) and urecholine 20-160 microgram./kg.hr.) which were made alone and with background infusions of cimetidine. Cimetidine acted competitively for acid output with histamine as the stimulus and noncompetitively for pentagastrin or urecholine. With histamine or pentagastrin pepsin was less inhibited than H+ and in the case of urecholine, pepsin secretion was not inhibited by cimetidine.
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PMID:Effect of cimetidine on stimulated gastric secretion and serum gastrin in the dog. 36 58

Gastric acid and pepsin output in response to 0.10 and 6.0 microgram . kg-1h-1 of pentagastrin response to complete elimination of the carotid baroreceptor discharge by cutting the bilateral sinus nerves. Such unloading of the baroreceptors simulates a blood pressure drop to 50--60 mmHg, resulting in a pronounced reflex increase in the activity of the sympatho-adrenal system. Cutting the sinus nerves caused an increased level of immuno-reactive gastrin in the portal plasma, and this elevated gastrin concentration was virtually extinguished by bilateral adrenalectomy. We conclude that the carotid baroreceptors can influence the gastrin release by a reflex adjustment of the release of adrenal catecholamines.
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PMID:Reflex adrenergic gastrin release evoked by unloading of carotid baroreceptors in cats. 37 Sep 67

1. In fasting anaesthetized cats pentagastrin and gastrin II, infused alone in doses which evoked a large acid response, did not stimulate the secretion of pepsin. However, peptic secretion increased significantly when either acid stimulant was infused simultaneously with a dose od Boots' secretin, in itself below the threshold for peptic stimulation. 2. The potentiation by pentagastrin and gastrin II of the peptic response to secretin was similar to the potentiation observed when caerulein, histamine and N-methyl histamine are given with secretin, an effect we have attributed to a non-specific increase of gastric mucosal blood flow which accompanies the infusion of these acid stimulants and effectively increases the concentration of secretin delivered at the site of the chief cell in the gastric mucous membrane.
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PMID:Pepsin secretion in anaesthetized cats stimulated by pentagastrin and gastrin II in the presence or absence of secretin. 37 2


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