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)

Lower esophageal sphincter pressure (LESP), basal gastric pH, and plasma levels of gastrin, estradiol, and progesterone were determined in ten women known to have normal menstrual cycles. All determinations were performed both during the follicular phase (Days 2 to 8) and during the luteal phase (Days 20 to 30). In addition, an intraluminal pH probe placed 5 cm. above the lower esophageal sphincter was used to test for the presence of acid reflux in response to three provocative procedures. LESP during the follicular phase was 19.0 +/- 1.5 mm. Hg (mean +/- S.E.M.) and during the luteal phase 16.5 +/- 1.3 mm. Hg (p less than 0.01). Basal gastric pH and plasma gastrin levels were similar at both times. Plasma estradiol in the follicular phase (76.1 +/- 7.0 pg. per milliliter) increased twofold during the luteal phase (159.0 +/- 6.0) (p less than 0.01). Plasma progesterone increased from a level of 1.5 +/- 0.8 ng. per milliliter during the follicular phase to 19.2 +/- 4.2 during the luteal phase. Coincident with these changes in LESP and increases in steroid levels, acid reflux was detected in five women during the luteal phase but was present in only one during the follicular phase.
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PMID:Lower esophageal sphincter pressure during the normal menstrual cycle. 3 79

Postnatal changes in the pH of gastric secretions, gastric motility, serum gastrin concentration, and response of the stomach to pentagastrin administration were studied in 15 beagle puppies from birth to 5 wk of age. Motility was monitored manometrically via twin-lumen catheters 3--6 h postprandially. Mean gastric pH was stable at 5.85 until the 7th postnatal day when pH decreased to 3.45; pH then increased to a mean value of 4.95 through the 18th day. Antral contractions increased from 0.2 contractions per min on the day of birth to a maximum 2.3 contractions per min on the 11th day and then gradually declined. Pentagastrin (8.0 microgram/kg sc) had no effect on gastric pH or motility until the 2nd postnatal wk. Pentagastrin inhibited the rate and peak pressure of antral contractions from the 2nd through the 5th wk. Mean serum gastrin concentrations in six puppies were greater than values for adult dogs, attaining a preweaning maximum on the 9th day.
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PMID:Neonatal gastric motility in dogs: maturation and response to pentagastrin. 3 82

The role of gastrin in the hormonal control of canine hepatic bile flow was evaluated. Because of the importance of the presence of sulfation of the carboxyl terminal peptide in the function of other cholecystokinetic hormones and peptides in the biliary tract, the choleretic properties of sulfated gastrin II were compared to the choleretic properties of nonsulfated gastrin I. Exogenous administration of gastrin I and II to dogs with chronic bile fistulas demonstrated that gastrin II, but not I, significantly increased hepatic bile flow. Chemical stimulation of the release of endogenous gastrin in dogs with denervated antral pouches did not increase hepatic bile flow, whereas a choleresis resulted when the innervated antrum was stimulated. Serum gastrin values obtained during the infusion of gastrin II at doses that produced a choleresis resulted in serum gastrin values that were greater than those produced by a more physiological stimulus, such as chemical antral stimulation. The results of this study suggest that only the sulfated gastrin II, not gastrin I, is a choleretic agent in dogs and only at pharmacological, not physiological doses.
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PMID:Effect of gastrin I and gastrin II on canine bile flow. 3 83

Measurements of serum epinephrine and gastrin, simultaneously, gastric mucosal blood flow and gastric secretion were carried out in cinchophen treated dogs. No significant changes in either serum concentrations of epinephrine and gastrin or fundic mucosal microcirculation after a single 100 mg/kg cinchophen administration were found while gastric secretion increased markedly after the medication. On the other hand, a significant increase in serum epinephrine and gastrin levels was observed while gastric secretion decreased significantly after large doses of cinchophen (300 mg/kg) were injected intravenously. Here gastric mucosal microcirculation is decreased. Repeated administration of 100 mg/kg cinchophen for 3 to 7 days brought about an increase in epinephrine and gastrin levels and caused an occurrence of fundic mucosal hemorrhage. Sympathetic discharge and gastrin release were not seen after a 3-week period of cinchophen administration. Cinchophen ulcers were produced, even when contact between the bile and the stomach mucosa was avoided. Vagotomy had no connection with ulceration and gastric secretion.
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PMID:Are epinephrine and gastrin accelerative factors of acute cinchophen ulcer?: Studies on gastric mucosal microcirculation and gastric secretion. 3 23

Plasma secretin, plasma gastrin and pancreatic bicarbonate output were measured in three healthy youths before and after a 10 min period of duodenal infusion of 50, 75 and 100 ml 100 mmol/1 HCl. Plasma secretin rose to a shortlived peak within 10 min, whereas plasma gastrin fell gradually to values significantly below the basal level 60 min after the start of duodenal acidification. Pancreatic bicarbonate output showed a more sustained increase following duodenal acidification. Significant positive correlations were obtained between plasma secretin and infused dose of HCl, between pancreatic bicarbonate output and infused dose of HCl and between plasma secretin and pancreatic bicarbonate output. The calculated maximal pancreatic bicarbonate output (Vmax) of 30.6 mEq/h and the calculated dose of secretin to elicit half maximal pancreatic bicarbonate output (S50) of 0.2 CU/kg-h following duodenal acidification were comparable to that seen after intravenous infusion of secretin. No significant correlation was found between plasma secretin and plasma gastrin. It is suggested that the pancreatic stimulation subsequent to duodenal acidification is mainly effected by release of secretin, and that the fall in plasma gastrin may be caused by a HCl-induced inhibition of gastrin release from the duodenum.
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PMID:The effect of duodenal acidification on plasma secretin and gastrin and pancreatic bicarbonate secretion in man. 3 87

A patient initially showed symptoms of peptic ulcer disease in 1953 and was later found to have hypercalcemia and hyperparathyroidism. Peptic ulcer symptoms persisted after parathyroidectomy, and results of studies provided evidence of the Zollinger-Ellison syndrome. Evaluation of the patient's family showed a classic pattern of multiple endocrine adenomatosis type 1. The patient underwent total gastrectomy and excision of a gastrin cell adenoma in 1971 with relief of symptoms, but with persistent hypergastrinemia. He remained in good health until January 1976, when symptoms of hypoglycemia developed. Results of laboratory studies were compatible with the diagnosis of a pancreatic beta-cell adenoma. At the time of operation, an adenoma of the head of the pancreas was found. The tumor was excised; no other metastatic tumors were found. The tumor was compatible with a beta-cell adenoma and was found to contain high concentrations of insulin; there was no important amount of gastrin. Symptoms of hypoglycemia have entirely disappeared.
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PMID:Separate pancreatic gastrin cell and beta-cell adenomas: report of a patient with multiple endocrine adenomatosis type 1. 3 17

The importance of beta-adrenergic and cholinergic mechanisms to the circadian rhythm of gastrins in serum was studied in 15 healthy volunteers. The subjects were investigated during peroral treatment with 1) a beta-adrenergic blocking drug (propranolol), 2) an anticholinergic drug (glycopyrron), 3) both drugs, and 4) without treatment. Gastrin concentrations were measured with an antiserum that measures all four main components of gastrin in serum, and with a gastrin-17 specific antiserum. A circadian rhythm was observed with both antisera. The total immunoreactivity in serum increased from 39 pg per ml +/- 3 (mean and S.E.M.) in the morning to a peak at 2300 (77 +/- 7), followed by a nadir at 0400 (38 +/- 2). The circadian rhythm was maintained during administration of the drugs, but the concentrations of component III (gastrin-17) were reduced by beta-adrenergic blockade, while the anticholinergic treatment increased the concentrations of the other gastrin components. The inhibition of gastric secretion of acid by anticholinergics is presumably due to an action on the parietal cells; according to this study, the inhibition is connected by an increased gastrin stimulus. Beta-adrenergic blockade, on the other hand, seems to reduce the gastrin stimulus and might be of therapeutical interest in duodenal ulcer disease.
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PMID:The effect of beta-adrenergic and cholinergic blockade on the circadian rhythm of gastrins in serum. 3 27

In conscious fullgrown minipigs simple SPV alone, SPV and pyloric stenosis and SPV and pyloroplasty were performed. After a liquid test meal the motoric and secretory function of the stomach were examined simultaneously by a modified method of intestinal perfusion and aspiration. After simple SPV initially a marked decrease of gastric volume and normal emptying into the duodenum were found. With additional pyloric stenosis no significant change was found. The pyloroplasty lead to an increase of gastric volume and delayed emptying. The acid secretion after feeding reduced by SPV was not changed significantly neither by pyloroplasty nor by pyloric stenosis. The baseline values of serum gastrin were elevated after SPV as well as after SPV in combination with pyloric stenosis or pyloroplasty. After food stimulation there was a delayed increase of gastrin after SPV which differed from that after SPV with pyloric stenosis or pyloroplasty only during the first hour. These results show that after SPV no further improvement of the motoric and secretory function can be achieved by an additional pyloroplasty. Furthermore these findings permit the conclusion that even after SPV with additional artificial pyloric stenosis no delayed gastric emptying occurs and that there is no negative effect postoperatively on the acid secretion and gastrin production.
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PMID:[Influence of pyloroplasty and pyloric stenosis on motoric and secretory function of the stomach after selective proximal vagotomy--an experimental study (author's transl)]. 4 77

The significance of antral pH for the basal serum level of immunoreactive gastrin and for the release of gastrin during insulin hypoglycemia has been studied in duodenal ulcer (DU) patients. To permit paired comparisons, 14 DU patients underwent two or three tests with insulin. Venous blood samples were collected at fixed intervals for determination of gastrin (radioimmunoassay). In the first insulin test, the gastric juice was aspirated; in the second test, the stomach was perfused with citrate-phosphate buffer, pH 7.0; and in the third test the stomach was perfused with 0.1M HCl, pH 1.0. The rate of buffer or acid perfusion was adjusted, and the pH of the perfusate was kept above 5.0 and below 1.3, respectively. Gastric perfusion with buffer or acid for 1 hour did not affect the basal serum gastrin level, nor did perfusion with buffer for 3 hours. Insulin hypoglycemia stimulated acid secretion and produced a significant integrated serum gastrin response during gastric aspiration, but the gastrin response was four times greater during buffer perfusion. Acid perfusion abolished the gastrin response. From our previous and present findings, it is concluded that the gastrin in serum during basal conditions is of extra-antral origin and is independent of antral pH. Insulin hypoglycemia releases antral gastrin by a pH-sensitive mechanism in DU patients; the release is suppressed at pH 1.3 or less and also is markedly inhibited when the gastric juice is aspirated.
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PMID:Significance of antral pH for gastrin release by insulin hypoglycemia in duodenal ulcer patients. 4 Mar 12

Isolated gastric glands of the rabbit were examined both with differential interference-contrast microscopy and with electron microscopy to describe the morphologic correlates of acid secretion. Stimulation of the glands with histamine resulted in the development of intracellular spaces within the parietal cells. A similar transformation was produced by addition of 1 mM aminopyrine, whether the weak base was added in the presence of normal-K+ (5.4 mM) or high-K+ (108 mM) solutions. The intracellular space was compatible with the expanded canaliculus described in stimulated parietal cells. Confirmation that the space produced by histamine is the site of acid secretion was gained by combining fluorescence and interference-contrast methods in the presence of the dye acridine orange, which displays a pH-dependent metachromasia in its emission spectrum. Human gastrin I resulted in an observable discharge of peptic granules.
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PMID:Cellular site of gastric acid secretion. 4 18


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