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 6 patients having duodenal ulcer disease plasma gastrin concentrations were determined before and after the oral administration of 0.5--2 g of calcium carbonate, 2--4 tablets of Camalox and 2 tablets of Novalucol. No significant influence on basal plasma gastrin levels was noted indicating that antacids, whether they contain calcium carbonate or not, do not influence the basal plasma concentration of gastrin at occasional administration.
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PMID:Effect of oral administration of calcium carbonate, Camalox and Novalucol on plasma gastrin concentration in duodenal ulcer patients. 76 Mar 93

Oral calcium carbonate (0-5 g, pH 9-4) increased serum gastrin and gastric acid output with slight but insignificant change in serum calcium. A similar rise in serum calcium during an intravenous infusion of calcium gluconate failed to increase serum gastrin and gastric acid output. Both intragastric calcium actions were abolished by acidification of the calcium carbonate solution (pH 1-0). The increase in serum gastrin and gastric acid output after intragastric calcium carbonate was not affected, however, by a simultaneous intraduodenal acid load. Equivalent neutralising doses of magnesium hydroxide (pH 9-4) did not increase serum gastrin and gastric acid output above basal levels, whereas antral acidification with 20 ml 0-1 N HCl resulted in a slight decrease in serum gastrin. Intraduodenal calcium carbonate (pH 3-0) also increased serum gastrin and gastric acid output, whereas an equivalent volume of intraduodenal saline (pH 3-0) had no effect. These findings indicate that calcium increases serum gastrin by local stimulation of antral and duodenal mucosa. They also suggest that the action of calcium on gastric secretion is partly mediated by gastrin.
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PMID:Calcium stimulation of gastrin and gastric acid secretion: effect of small doses of calcium carbonate. 87 25

In rats given a copper-deficient diet plus penicillamine to destroy the acinar tissue selectively, the sensitivity and secretory pattern of pancreatic duct cells to a variety of hormones has been investigated. Resting flow rate of this pancreatic duct model was in the same range as in the intact gland. The duct cells responded to increasing doses of secretin by producing more juice with increasing outputs of bicarbonate, sodium, potassium, and chloride. Bicarbonate concentration increased with the lowest dose of secretin up to values of 64 mEq per liter and did not further increase with higher doses of secretin and increasing secretory rates. The concentration of potassium increased with increasing doses of secretin and flow rates, whereas chloride concentration decreased in a reciprocal fashion to bicarbonate. Gastrin and cholecystokinin-pancreozymin did not significantly stimulate the duct cells. Atropine did not inhibit the action of secretin on the flow rate or on bicarbonate secretion.
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PMID:Pancreatic duct cells in rats: secretory studies in response to secretin, cholecystokinin-pancreozymin, and gastrin in vivo. 90 83

Basal gastrin and acid secretion, and histamine- and food-stimulated acid secretion were examined before and after 6 weeks of regular antacid consumption by 20 normal volunteers, in order to test the hypothesis that regular use of antacids produces gastrin cell hyperplasia, altered gastrin inhibition by acid, and gastric hypersecretion. We found no differences in fasting serum gastrin, basal or maximal histamine-stimulated acid, or acid output in response to a protein meal after consumption of commercial antacids with or without calcium carbonate. The results suggest that normal subjects do not acquire functional hyperactivity of the gastrin mechanism after a period of regular antacid use.
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PMID:Effect of chronic antacid ingestion on serum gastrin and gastric secretion. 101 94

Calcium gluconate, carbonate, and lactate are potent antiulcerogenic agents when administered intragastrically at pH 6.3 by sustained infusion (45 mg/kg/8 h). In intact rats, by radioimmunologically measurable serum, gastrin and calcitonin are inversely correlated, whereas gastrin and ulcer index tend to correlate directly. The findings imply a key role for thyroid-releasable endogenous calcitonin in this disorder.
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PMID:[Calcium in the prevention of stress ulcer in the rat]. 103 6

The effect of bombesin on external pancreatic secretion was studied in seven healthy volunteers and intwo patients with a two-thirds gastrectomy and a pancreatic fistula. After bombesin infusion (15 ng/kg/min), gastrin levels were significantly raised in all volunteers, but remained at basal levels in the gastrectomized patients. Bombesin was effective in stimulating pancreatic secretion in all patients. The volume of secretion increased tow-fold when compared with basal volume. Amylase and trypsin concentrations and outputs in the duodenal juice were greatly agumented (amylase concentration: basal, 70 dye U/ml; post-bombesin, 620 dye U/ml. Amylase output: basal, 1000 dye U/15 min; post-bombesin, 15,800 dye U/15 min). Secretin, when administered in conjunction with bombesin, partially inhibited its secretory effect. Bicarbonate secretion was slightly stimulated by bombesin, but at a very low level. A similar pattern of results was obtained in the two gastrectomized patients. In man, bombesin exerts an effect on pancreatic secretion that mimics the effect of CCK-PZ, thus confirming the results obtained in the experimental animal. Gastrin does not play a fundamental role in this phenomenon.
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PMID:External pancreatic secretion after bombesin infusion in man. 121 23

We review acid rebound, the seemingly paradoxical increase in acid secretion resulting from administration of an antacid. Primarily a laboratory observation, the demonstration of the phenomenon was a major contributing factor to the swift, and possibly unjustified, fall from grace of calcium carbonate in the therapy of peptic ulcer disease despite years of apparently successful use. Calcium, as carbonate or other salts, causes an increase in gastric acid secretion owing, at least in part, to direct ionic stimulation. Another possible mode of action involves antral alkalinization with subsequent gastrin release. Other antacids, notably magnesium hydroxide and aluminum hydroxide, may therefore also cause rebound, but the data in this area are less convincing. Despite the demonstration that acid rebound occurs, no one has thoroughly investigated its clinical import. What limited data actually exist suggest no obvious clinically significant deleterious effect from use of calcium carbonate in peptic ulcer. Because of calcium carbonate's excellent acid-neutralizing capacity, its venerable past record in treating ulcer disease, and recent observations that low-dose antacids heal peptic ulcers, it is appropriate to reevaluate acid rebound, to focus on its clinical significance, if any.
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PMID:Calcium and acid rebound: a reappraisal. 150 Jun 60

The effects on pancreatic responses of highly potent cyclic hexapeptide (cyclo (N-Me-Ala-Phe-D-Trp-Lys-Thr-Phe)) (Veber analog) and octapeptide analogs of somatostatin such as D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Thr-ol (SMS 201-995), D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Thr-NH2 (RC-121), and D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) have been compared with somatostatin tetradecapeptide (SS-14) and atropine. The parameters evaluated were pancreatic responses to secretin and meat feeding in conscious dogs with chronic pancreatic fistula and amylase release from the dispersed pancreatic acini. The analogs were administered intravenously or intraduodenally. The cyclic hexapeptide and octapeptide analogs, given iv in graded doses against a constant background stimulation with secretin, produced similar and dose-dependent inhibition of pancreatic HCO3- and protein secretion. Analogs RC-121, RC-160, and the Veber analog were about two to four times more active than SS-14 in suppressing HCO3- secretion and equipotent in reducing protein secretion, but SMS 201-995 was only about half as potent as somatostatin in inhibiting HCO3-. RC-160 was effective in inhibiting secretin-induced protein secretion at lower doses than other analogs. In tests with feeding, SMS 201-995, the Veber analog, RC-121, and RC-160 were more potent inhibitors of exocrine pancreatic secretion of HCO3- and protein and exhibited more prolonged inhibitory effects than SS-14. The Veber analog, RC-121, and RC-160 were also more effective after intraduodenal administration. Atropine also caused significant inhibition of both HCO3- and protein responses to secretin and meal feeding. All four analogs decreased the postprandial insulin and pancreatic polypeptide release to a similar degree as SS-14. Neither SS-14 nor the analogs tested significantly affected basal or caerulein-, gastrin-, secretin-, or bethanechol-stimulated amylase release from the dispersed canine pancreatic acini. Atropine reduced amylase release induced by bethanechol, but not that stimulated by caerulein, gastrin, or secretin. This indicated that the analogs, as somatostatin, are ineffective as secretory inhibitors in vitro. We conclude that cyclic hexapeptide and octapeptide analogs are more potent and longer acting inhibitors of pancreatic secretion than somatostatin-14 in vivo.
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PMID:Comparison of somatostatin and its highly potent hexa- and octapeptide analogs on exocrine and endocrine pancreatic secretion. 244 2

Experimental studies located carbonic anhydrase (CA) in the parietal cells close to secretory canaliculi, in superficial epithelial cells and gastric microvasculature. The role of CA is CO2 hydration resulting H+ for acid secretion and conversion of OH into HCO3-. Our studies showed that the physiological secretagogue histamine, acetylcholine and gastrin are all CA activators, achieving potentiating interactions. Catecholamines are also strong enzymatic activators. Beside sulfonamides, other CA inhibitors are anticholinergics, PGE and PGI2, some calcium channel blockers, alpha 2- and beta 1-adrenoceptor blockers and Zn2+. Cytoprotective properties of CA inhibitors gained experimental evidence in the past years. These effects could be based on increase of gastric mucosal blood flow, proved experimentally, which might be mediated by increase of endogenous prostaglandin synthesis and sulfhydryls and, respectively, motility changes. The unique combination of strong antisecretory effect with the cytoprotective action explain the outstanding clinical efficacy of CA inhibitors in the healing of gastric and duodenal ulcers.
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PMID:Carbonic anhydrase inhibitors: antisecretory and cytoprotective properties. 251 64

A few recent reports suggest the protective effect of antacids against gastric mucosal injury. This study was aimed to examine the influence of some antacids on ethanol induced gastric mucosal damage in rats. We have found that Polish antacids (Alugastrin, Gelatum Aluminii Phosphorici, Gastrin) and calcium carbonate diminished gastric mucosal lesions produced by ethanol. Moreover, Alugastrin and Gelatum Aluminii Phosphorici decreased volume of gastric contents, and its pH, as well as lowered sodium, potassium and protein levels and decreased LDH activity in gastric contents. These findings indicate that antacids protect rat gastric mucosa against injury caused by ethanol. We have found also that aspirin given prior to Alugastrin abolished the protective ability of Alugastrin. This suggest that prostaglandins might be involved in antacid cytoprotection. Our studies indicate that antacids can be used prophilactically in the gastric mucosal injuries.
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PMID:[Protective effect of alkalies on ethyl alcohol-damaged gastric mucosa]. 264 41


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