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)

Components of a histochemical method for demonstrating carbonic anhydrase activity have been investigated quantitatively. It was found that it is not necessary to use free-floating sections provided the reaction is done in a reaction medium of controlled depth. This permits the use of normal cryostat sections on glass slides, so making this technique applicable to the cytochemical bioassay of gastrin. The better control of the pH of the reaction, and changes in the concentration of phosphate and of cobalt, have resulted in a quantitatively reproducible reaction in the parietal cells of guinea-pig fundus. The reaction product is measured by microdensitometry. The specificity of the carbonic anhydrase reaction has been tested by the response elicited by gastrin acting on the parietal cells in vitro and by the use of acetazolamide.
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PMID:A quantitative cytochemical method for measuring carbonic anhydrase activity. 2 56

In acute experiments on cats antral pouches were perfused with solutions of different pH (1-13). After antrum passage the gastrin levels in the perfusates were measured with radioimmunoassay and the amounts of gastrin released into the antral lumen per minute calculated. The venous gastrin levels were determined concomitantly. Small amounts of gastrin (1,000--1,500 pg/min) were released into the antrum during perfusion with 0.1 M HCl. Subsequent perfusion with 0.15 M NaCl (pH 6.8) did not significantly increase the release of gastrin. On the other hand, 0.1 M phosphate buffer (pH 7.4) caused a dramatic augmentation of the gastrin output into the antral lumen (approximately 17 fold). A concomitant increase of peripheral gastrin levels was observed. Also other alkaline solutions such as 0.15 M NaHCO3 (pH 8), 0.15 M Tris buffer (pH) or 0.01 and 0.1 M NaOH (pH 12 and 13) promoted the release of gastrin. It is discussed whether the gastrin release at alkaline pH is induced by the alkaline pH itself or by anions such as HPO-4, HCO-3 and OH-. The apparent effect of pH could then be due to the formation of these ions at higher pH.
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PMID:Effect of intraantral pH on basal gastrin release into the circulation and antral lumen in anesthetized cats. 3 63

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

The effect of variations of intra-antral pH on the intraluminal release of somatostatin was studied. Acute pouches were created in anaesthetized cats, and the pouches were perfused with solutions differing in pH. Somatostatin levels were then measured in the perfusates. In this model phosphate buffer was a potent stimulator of intra-antral somatostatin release, whereas perfusion with 0.1 M HCl failed to release somatostatin by itself. Since phosphate buffer also releases gastrin, the releasing effect ought to be exerted beyond the mechanism that can be blocked by somatostatin. (Thus the stimulatory effect of phosphate buffer might be exerted on the membranes of the endocrine cells.)
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PMID:Phosphate buffer stimulates somatostatin release into the antral lumen of anaesthetized cats. 4 3

A case of watery diarrhea, hypokalemia and hypercalcemia associated with an islet cell tumor was described. A 62-year old man exhibited frequent watery diarrhea and hypokalemia for two years. He had no peptic ulcer and serum gastrin level was normal. His serum calcium was abnormally high and serum phosphate was lowered. He had secretin-like activity in his plasma. Autopsy revealed a small islet cell tumor in the pancreas and several metastatic masses in the liver. Microscopic examination revealed the tumor cell was not beta, alpha nor D cells. By electron microscopy the secretion granules of the tumor cell resembled those of S, M and T cells. It was not possible to decide which of the tree cell types was responsible for the pancreatic cholera.
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PMID:A case of watery diarrhea, hypokalemia and hypercalcemia associated with nonulcerogenic islet cell tumor of the pancreas. 17 23

High levels of serum calcitonin were found in patients with chronic renal failure. Serum calcitonin correlated directly with the phosphate to total calcium ratio; calcitonin levels correlated inversely with serum calcium in those patients on dialysis and directly with serum calcium in nondialysis patients. All patients had elevated serum gastrin. The high levels of serum calcitonin usually decreased following successful kidney transplantation. The pathophysiology of this hypercalcitonemia and its relationship to renal osteodystrophy and the disordered calcium metabolism of uremia remains to be elucidated.
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PMID:Calcitonin levels in chronic renal disease. 33 Nov 28

Antral somatostatin- and gastrin-producing cells (D and G cells) were studied in a group of patients with chronic renal failure (CRF) in comparison with a control group. Gastric acid secretion and serum gastrin, phosphate, and parathormone (PTH) levels were also evaluated in every patient. The group with CRF showed a mild increase both in G- and in D-cell denisty. In this group serum phosphate and PTH levels were higher than normal, showing hyperparathyroidism in every patient. A direct correlation was found between G-cell density and parathyroid function in patients with CRF. Hyperparathyroidism, therefore, seems to play a role in the mechanism of increased serum gastrin levels in CRF.
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PMID:Antral G- and D-cell counts in chronic renal failure. 37 75

Whisky (25-50 ml) increased plasma levels of immunoreactive calcitonin (iCT) in seventeen of nineteen patients with chronic renal failure. The effect was greater in patients with high levels of iCT than in those with normal levels. Changes in plasma iCT were not related to changes in calcium, phosphate or immunoreactive gastrin, but were inhibited by the prior administration of propranolol.
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PMID:Ethanol induced secretion of calcitonin in chronic renal disease. 42 14

The influence of restraint stress on serum calcium (Ca) and phosphate was studied in normal and thyroidectomized rats. In addition the response of gastric stress ulcer index, blood gastrin and glucagon to exogenous Ca was investigated. In intact as well as in thyroidectomized animals serum total, ionised and previously injected radioactive Ca decrease during an 8h stress period, whereas inorganic phosphate increases. Together with a constant specific activity these findings are consistent with hypoparathyroidism and calcitonin independent hypocalcemia during stress. Intragastric infusion of 45 mg/kg Ca-gluconate per 8h proves to be a potent anti-stress ulcer regimen in intact and neck-sham operated, but not in thyroidectomized rats without and with additional adrenal demedullation. Gastrin and glucagon were not correlated with calcemia during either stress alone or stress combined with intragastric Ca infusion. It is suggested that the development of gastric stress ulcerations can be prevented by a Ca-mediated release of endogenous calcitonin.
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PMID:Hypocalcemia during restraint stress in rats. Indication that gastric ulcer prophylaxis by exogenous calcium interferes with calcitonin release. 47 75

The purpose of this study was to evaluate the effect of histamine phosphate and specific histamine antagonists on human lower esophageal sphincter (LES) pressure. Continuous intravenous infusions of histamine at doses of 2.0 to 40.0 microgram/kg-hr gave graded increases in LES pressure with a peak response of 378 +/- 4.6 mm Hg at 20.0 microgram kr-hr. The LES response was not altered by an H1-antogonist, diphenhydramine (50 mg, intravenously), but was completely blocked by infusion of the H2-antagonist, cimetidine (4.0 mg/kg-hr). Also, oral cimetidine (300 mg) antagonized any increase in LES pressure during histamine infusion at a dose shown to give the maximal LES response. Despite this effect of cimetidine in antagonizing the maximal LES response to histamine, oral cimetidine at 200, 300, and 400 mg failed to alter basal LES pressure over a 3-hr period. Cimetidine also failed to alter the LES response to intravenous pentagastrin or oral beef hydrolysate. These studies suggest that: (1) human LES pressure increases in response to intravenous histamine phosphate through its action at an H2-receptor; (2) the H1-receptor has no apparent role in the human LES response to histamine; and (3) H2-antagonism with cimetidine has no effect on the human LES basal pressure or its response to gastrin stimulation.
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PMID:Effect of histamine and histamine antagonists on human lower esophageal sphincter function. 62 Sep 12


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