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)

Smokers have an increased incidence of duodenal ulcer with a high relapse rate whether they receive maintenance therapy with H2-receptor antagonists or not. They also tend to be slow healers. The etiology behind this is still unknown, and there is general disagreement as to whether smoking affects gastric secretion. In an earlier study we found a small but significant decrease in intragastric pH a short time after smoking a cigarette. The aim of the present investigation was to study whether intragastric pH changed during nicotine administration per se. Nicotine was given as a nasal spray to eight healthy smokers. Nicotine did not induce any acute detectable changes in gastric acidity when the 5-min period before spraying was compared with the 35-min period after spraying (median pH, 1.47 (25-75 percentiles, 1.40-2.32) and 1.55 (25-75 percentiles, 1.42-2.06), respectively). When different time periods during a day with hourly nicotine administration were analyzed, and the results compared with those of a similar day when placebo was given, nicotine was found to impair postprandial gastric neutralization. Median pH during the lunch hour was 1.93 (25-75 percentiles, 1.80-2.37) after nicotine and 2.86 (25-75 percentiles, 2.37-3.70) after placebo; p less than 0.025. Possible explanations for this might be nicotine-mediated effects on gastric motility or gastrin release.
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PMID:Does nicotine administration influence intragastric acidity? 156 29

The effects of bombesin and gastrin releasing peptide (GRP) on the release of catecholamine were investigated by using isolated rat adrenal gland. Bombesin and GRP stimulated an epinephrine (E) release with dose-dependency. A half maximal effect of bombesin was observed at 1.2 X 10(-9) M, and a maximal release of E occurred at 1 X 10(-6) M of bombesin. The stimulatory effect of GRP on the E release was very similar to that of bombesin. Although both these peptides also stimulated a norepinephrine (NE) release, a significant effect was detected at concentrations of bombesin and GRP above 1 X 10(-7) M. Nicotine and pilocarpine stimulated both E and NE releases dose dependently, but the effect of pilocarpine on E and NE release was 1/100 or less potent than that of nicotine. Bombesin-induced catecholamine releases were not inhibited by hexamethonium or atropine that fully impeded the stimulatory effects of nicotine or pilocarpine. In addition, bombesin had additive effects on the nicotine- or pilocarpine-induced E and NE releases. These data strongly suggest that bombesin or GRP plays a physiological role as one of the important regulators in catecholamine secretion in the adrenal gland.
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PMID:Effects of bombesin and gastrin releasing peptide on catecholamine secretion from rat adrenal gland, in vitro. 286 24

Smoking has an unfavourable effect on peptic ulcer disease. The pathophysiological mechanisms underlying this effect are not known. The enterochromaffin like (ECL) cell is the cellular source of histamine participating in the regulation of acid secretion. The ECL cell is under functional and trophic control of gastrin and the vagus nerves. Nicotine may affect acid secretion through vagal pathways. Furthermore, nicotine may also stimulate neuroendocrine cells. The present study examined if chronic nicotine administration could stimulate the function and growth of the ECL cell. Rats inhaled nicotine vapour at a concentration of approximately 6.2 mumol/m3, 20 hours/day, 5 days/week for 11 weeks. Steady state plasma nicotine concentration was 461.8 (137.5 (SD)) nmol/l. The ECL cell density, histamine content and histidine decarboxylase activity of the oxynitic mucosa were similar to the controls. We also examined the effect of acute nicotine stimulation on the acid output and histamine release from the totally isolated vascularly perfused rat stomach. Nicotine did not stimulate acid secretion or histamine release. Thus no evidence could be provided to support the hypothesis that nicotine exerts its negative effects on peptic ulcer disease by stimulating the ECL cell.
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PMID:Effect of nicotine on the enterochromaffin like cells of the oxyntic mucosa of the rat. 768 47

The effects of chronic nicotine treatment on gastric acid secretion stimulated by subcutaneous injection of pentagastrin, as well as on serum gastrin levels and the stomach parietal cell population, were examined. Rats drank a solution of nicotine 25 micrograms/mL tap water for periods of 10, 30 or 45 days. Pentagastrin increased the gastric secretory volume and acid output in pylorus-ligated control animals that drank tap water. Animals given nicotine in their drinking water for 10, 30 or 45 days showed increased basal gastric secretion and acid output. Pentagastrin produced maximum stimulatory effects at lower dose levels of 50 micrograms/kg in the 10-day treatment group and 25 micrograms/kg in the 30- or 45-day treatment groups; however, the maximum responses to pentagastrin in all nicotine-treated batches were comparable to those of their corresponding controls. Serum gastrin levels remained unchanged from the 10th day of nicotine treatment, whereas the levels in the control animals continued to rise with age. Nicotine 25 micrograms/mL drinking water given for 10, 30 or 45 days caused no significant changes in the parietal cell population, mucosal surface area or mucosal thickness. These findings are consistent with the idea that chronic nicotine administration, for at least 10 days, will lead to increased muscarinic receptor sensitivity; basal acid secretion is consequently elevated, and this in turn may depress gastrin secretion.
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PMID:The contrasting influence of chronic nicotine intake on gastrin and gastric acid secretion. 896 34

The purpose of this study is to examine the effect of nicotine on famotidine-induced hypergastrinemia in the rat. In addition, the effects of nicotine on gene expression for gastrin and chromogranin A (CGA) in the stomach were examined. Famotidine treatment alone (20 mg/kg. 2 x/day for 14 days) increased serum gastrin levels significantly (P < 0.05) but not antral levels of gastrin mRNA and peptide. Nicotine treatment (12 mg/kg/d) alone did not affect serum gastrin levels; however, nicotine potentiated the hypergastrinemic action of famotidine. The hypergastrinemic action of nicotine was not mediated by a downregulation of stomach somatostatin (SRIF) since stomach SRIF mRNA levels were unaffected by nicotine treatment. Administration of nicotine and famotidine also upregulated stomach CGA gene expression (i.e., mRNA and protein levels) significantly.
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PMID:Interaction of nicotine and a H2-receptor antagonist, famotidine, on gastrin and chromogranin A expression. 917 49