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 effect of H2-receptor blockade on intragastric acidity was studied in nine normal males. The pH of their gastric contents was measured at hourly daytime and two hourly nighttime intervals for 48 hours. The subjects ate identical meals, drank identical volumes of fluid, and smoked the same number of cigarettes during the two study days. Their physical activity was unrestricted in a ward environment. Blood cimetidine and plasma gastrin were measured in serial blood samples. The nine subjects were treated in random sequence with cimetidine 0-8-1-0 g on one day and placebo capsules on the other. The drug was given in four divided doses: four subjects received it before, and five after, the three main meals. All took the fourth dose at bedtime. Replicate studies in an additional subject given placebo on both study days showed good reproducibility (r=0-80, P less than 0-01). Cimetidine therapy decreased intragastric acidity in all nine subjects. The decrease was similar in the two groups taking the drug before or after meals, mean 24 h intragastric hydrogen ion activity being lowered by 70 and 72% respectively. Nocturnal anacidity was recorded in only two of 45 samples. Administration of cimetidine before meals produced earlier and higher drug blood levels than post-prandial medication, but when it was taken after food the blood levels were highest at the time when the buffer capacity of the food was waning. Blood concentrations of cimetidine exceeded the secretory IC50 level for most of the time between doses. The results show that cimetidine 0-8-1-0 g/day in four divided doses produces a striking and consistent decrease of intragastric acidity. Although variation in the timing of the dose in relation to meals did not affect the decrease of acidity, the absorption data suggest that patients should take the drug after meals.
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PMID:Effect of cimetidine on 24-hour intragastric acidity in normal subjects. 0 61

In five conscious dogs with gastric fistula and two duodenal cannulas, plasma RIA secretin and gastrin levels were determined in response to 1) infusion of 0.1 N HCl in the proximal duodenal cannula, 2) ingestion of a meal, and 3) intraduodenal infusion of 0.1 N HCl following ingestion of a meal. Significant increases in plasma RIA secretin levels occurred during duodenal acidification. However, no significant change occurred in the secretin levels after ingestion of a meal, whereas significant increase in plasma gastrin level was observed. Postprandial duodenal pH remained above 4.5 for 3 h.
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PMID:Plasma secretin and gastrin responses to a meat meal and duodenal acidification in dogs. 0 78

The mechanisms controlling secretion of glucagon and other pancreatic hormones were studied in a patient affected with multihormone-secreting islet-cell tumor. Fasting glucagon levels (3,000 pg./ml.) rose to 10 ng./ml. following arginine stimulation. While oral glucose load and intravenous glucose infusion did not suppress glucagon secretion, insulin administration induced a prompt depression in glucagon levels. Glucagon, insulin, and gastrin levels were suppressed by somatostatin while calcium infusion caused a paradoxical increase. It is suggested that only some of the stimulation-inhibition mechanisms were conserved in this case of glucagon-secreting pancreatic tumor.
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PMID:Suppression and stimulation mechanisms controlling glucagon secretion in a case of islet-cell tumor producing glucagon, insulin, and gastrin. 0 26

The effect of cimetidine, a new histamine H2-receptor antagonist, on gastric acid secretion stimulated by a homogenised meal was studied in six normal volunteers using an in vivo intragastric titration technique. The subjects were studied twice, no more than 48 h apart, receiving either cimetidine 200 mg or placebo in random order. Cimetidine administered either 32 men before (three subjects) or with the meal (three subjects) significantly inhibited gastric acid secretion in all the subjects throughout the period of study; 96 min after food, total acid secretion decreased by 67 and 57% respectively. When the drug was taken with the meal absorption was slower (mean peak blood level 2-34 mumol/l, 80-128 min after dosing) than when administered on an empty stomach (mean peak blood level 5-08 mumol/l, 48-64 min after dosing). Blood cimetidine concentration correlated significantly (P less than 0-01) with percentage inhibition of acid output and the calculated concentration resulting in 50% inhibition of gastric acid secretion (IC50) was 1-6 mumol/l. Secretion of gastrin in response to food was unaffected by cimetidine. The results suggest that 200 mg cimetidine effectively inhibits food-stimulated acid secretion and that the bioavailability of the drug may be affected by the timing of dosage in relation to meals. No unwanted effect were observed.
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PMID:Inhibition of food-stimulated gastric acid secretion by cimetidine. 0 42

Meal-stimulated acid secretion, measured by in vivo intragastric titration, was progressively inhibited by increasing oral doses of cimetidine (25 to 400 mg). Four hundred milligrams suppressed acid secretion by 73% for the first 3 hr after the meal, whereas it inhibited acid secretion by 94% during the 30-min period of maximal inhibition. The dose of cimetidine required to suppress acid secretion by 50% during the 30-min period of maximal inhibition was 25 mg. The duration of action of a 300-mg dose was at least 7 hr. Cimetidine was equally effective in inhibiting meal-stimulated acid secretion at two physiological intragastric pH levels (5.0 and 2.5). Cimetidine had no effect on serum gastrin concentration when intragastric pH was maintained at 5.0, but when pH was allowed to seek its own level, serum gastrin concentration was higher after cimetidine than after placebo. Cimetidine had no effect on gastric emptying. No side effects were noted in any patients.
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PMID:The effect of cimetidine, a new histamine H2-receptor antagonist, on meal-stimulated acid secretion, serum gastrin, and gastric emptying in patients with duodenal ulcer. 0 59

In 10 normal subjects, in 32 patients with duodenal ulcer (DU), and in 11 patients with partial gastrectomy (Billroth I), serum gastrin rose significantly after an oral and intraduodenal test meal. The highest increases were observed in DU patients after the oral as well as after the intraduodenal test meal. After the intraduodenal test meal in 4 normal subjects and in 17 DU patients an increase of gastric acid secretion and serum gastrin was measured. In basal state, after an intraduodenal or an oral test meal, DU patients with normal gastric acid secretory capacity had higher serum gastrin concentrations than DU patients with gastric hypersecretion. There was a good correlation between peak serum gastrin levels after the oral and after the intraduodenal test meal. From these data it is concluded: (1) Intraduodenal application of a test meal results in release of gastrin from extragastric sites. (2) Extragastric gastrin is biologically active. (3) DU patients are able to release more antral and more extragastric gastrin in response to a test meal. Further studies, however, are necessary to show the significance of these findings in the pathogenesis of peptic ulcer disease.
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PMID:Gastric and extragastric gastrin release in normal subjects in duodenal ulcer patients, and in patients with partial gastrectomy (Billroth I). 0 56

Specific binding of radiolabeled gastrin by gastric mucosal cells prepared from guinea pigs was detected and examined. Specific cell binding of gastrin was found to be both pH and temperature dependent. Maximum binding of radiolabeled gastrin by gastric mucosal cells was demonstrated at pH 7.4 and at 4 degrees C. Substantial degradation of 125I-gastrin occurred during incubation with gastric mucosal cells. Gastrin degradation was detected both by loss of immunological reactivity with antibodies to gastrin and by abolition of subsequent specific binding after prior incubation with gastric mucosal cells. Degradation of gastrin was most marked with incubations conducted at pH 7.4 and at low pH (pH 2.0), suggesting the activities of at least two gastrin-degrading enzyme systems in the gastric mucosal cell preparation.
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PMID:Degradation of gastrin by gastric mucosal cells. 0 73

1. Both gastrin and the vagus nerve play a part in the pathogenesis of the duodenal ulcer. Which of these two factors is of greater significance--this problem is still subject to discussion as is the question whether other factors such as duodenal neutralization are more important than hitherto assumed. 2. At this time no reliable and harmless drugs that speed up the healing of duodenal ulcers and prevent relapses are yet available. Candidates for this are H2 receptor blockers, prostaglandines and possibly substances resembling secretin. 3. Only some of the participants considered it necessary to do endoscopic and radiological follow-ups in duodenal ulcers. 4. Proximal gastric vagotomy for the treatment of duodenal ulcers is still undergoing clinical trials. At present this method should only be used by surgeons with a special interest in gastric surgery who also dispose of the technology and the staff for careful postoperative checks on these patients. The advantages of proximal gastric vagotomy consist in sparing truncation, low mortality and good functional results. 5. In gastric ulcers--contrary to duodenal ones--malignancy should always be suspected. If medical treatment does not lead to complete remission within a few months, surgery must be performed. 6. Many surgeons still prefer resection to vagotomy and excision in the management of gastric ulcers.
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PMID:[Round table discussion. Ulcer - vagus - gastrin]. 0 81

Histamine H2-receptor antagonists, including burimamide, metiamide and cimetidine, are effective antagonists of histamine-stimulated acid secretion from mammalian, avian or reptilian gastric mucosa. Acid secretion stimulated by gastrin or pentagastrin is also inhibited by these drugs, but there is disagreement about the effects of these drugs on acid secretion resulting from activation of acetylcholine receptors. Based on the pharmacological evidence possibilities of treatment by these drugs were discussed in cases with excessive stimulation of acid secretion due to high blood levels of histamine or gastrin. The positive results in several trials on Zollinger-Ellison syndrome and peptic ulcer were very impressive. Some practical problems have still to be solved, for example the appropriate phase for applying the drugs. The demonstrated clinical effectiveness, however, against peptic ulceration offers a clear alternative to surgery for many patients.
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PMID:Histamine H2-receptor antagonists and gastric acid secretion -- a progress report. 1 Apr 67

Cimetidine infusion (100 mg h-1) reduced the acid secretory response to insulin infusion (0.03 units Kg-1h-1) when compared to paired control tests in 6 healthy volunteers. There was no significant difference between cimetidine and control tests in terms of pepsin output or serum gastrin concentrations. Cimetidine also reduced the acid secretory response when administered after 90 minutes of insulin had established a secretory response in extended tests in 3 additional volunteers. Cimetidine may have therapeutic potential in the peptic ulcer diathesis.
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PMID:Effect of the histamine H2-receptor antagonist, cimetidine, on gastric secretion and serum gastrin during insulin infusion in Man. 1 Jun 20


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