Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Caerulein is a decapeptide which combines the effects of gastrin and cholecystokinin-pancreozymin. It was injected intravenously in doses of 10 to 40 nanoponds caerulein per kilopond bodyweight in 37 patients and roentgen kymography of the stomach carried out before and after the injection. In 89% of the 36 cases which could be evaluated, it increased antral peristalsis. Amplitude and frequency were increased and the periodicity decreased correspondingly. The effect was more marked than that of pentogastrin, presumably because caerulein dose not affect duodenal acidity. The changes in motility therefore correspond with those produced by serotonin and cholecystokinin-pancreoxymin. Control examinations carried out under identical conditions, but without caerulein, showed no change in antral peristalsis.
 ...
PMID:[Roentgen kymographic investigations of gastric peristalsis after intravenous injection of caerulein]. 12 10

The fasting serum cholecystokinin-like activity was measured in 21 infants with pyloric stenosis and in 13 normal controls. No significant difference was found between the two groups. The basal acid secretion was measured by continuously aspirating the previously emptied stomach for one hour. The basal gastric volume and the total and the free acidity were all greater in the pyloric group.
 ...
PMID:Serum cholecystokinin, basal acid secretion, and infantile pyloric stenosis. 50

In order to investigate the vagal afferent pathway responsible for the previously reported effects of cholecystokinin (CCK) on gastric emptying and food intake, single afferent fibres were recorded from the cervical vagus of urethane-anaesthetized ferrets. Sixty tension receptor afferents with receptive fields in the corpus, antrum, duodenum, jejunum and ileum all showed a resting level of discharge which was augmented powerfully by distension of the segment containing the ending. Close intraarterial injection of CCK-8 (100-200 pmol) caused relaxation in proximal regions, but enhanced contractile activity in more distal regions. Mechanoreceptor discharge closely followed intraluminal pressure at all times, indicating a sensitivity primarily to tension and no direct sensitivity to CCK. Only duodenal tension receptors were significantly excited by CCK (due to increased contractile activity), whereas those in the stomach showed a net decrease. Thirty-seven mucosal receptors from the corpus, antrum, duodenum and jejunum showed responses to luminal stimuli: predominantly light stroking, acidity and hypertonicity as has been previously described. No responses to glucose or amino-acid infusions could be evoked. However, mucosal fibres showed a strong sensitivity to close-intraarterially injected CCK-8 (3-200 pmol) in 19/26 fibres tested. These responses were unaffected by cholinergic blockade when tested. The data strongly suggest that in the ferret only vagal mucosal receptors are directly sensitive to CCK-8. These fibres are therefore likely candidates for mediating some of the reflex and behavioural effects of CCK when it is released from the gastrointestinal tract and acts directly on vagal sensory endings.
 ...
PMID:Effects of cholecystokinin (CCK-8) on two classes of gastroduodenal vagal afferent fibre. 208 84

We have purified an acidic octapeptide from the neural ganglion of the protochordate Ciona intestinalis by a three-step procedure including C18 Sep-Pak fractionation, MonoQ ion-exchange chromatography, and C4 reversed-phase high-performance liquid chromatography. The purification was monitored by an immunoassay specific for the alpha-carboxyamidated COOH terminus common to the mammalian brain-gut hormones, cholecystokinin and gastrin. Automated Edman degradation revealed the sequence Asn-Tyr-Tyr-Gly-Trp-Met-Asp-Phe. In accordance with the high acidity of the peptide, amino acid analysis after cleavage with aminopeptidase M showed that both tyrosyl residues are sulfated. Hence, the structure is Asn-Tyr(SO3)-Tyr(SO3)-Gly-Trp-Met-Asp-Phe-NH2, as also confirmed by identity with the synthetic disulfated peptide in different chromatographic systems. The occurrence of two consecutively sulfated tyrosyl residues after a neutral residue challenges present concepts of consensus sites for tyrosyl sulfation. We conclude that the structure of the peptide, named cionin, suits that of a common ancestor for cholecystokinin and gastrin.
 ...
PMID:Cionin: a disulfotyrosyl hybrid of cholecystokinin and gastrin from the neural ganglion of the protochordate Ciona intestinalis. 230 39

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.
 ...
PMID:[Clinical characteristics of bile reflux gastritis]. 273 41

In 27 infants aged 20 to 65 days with clinically and roentgenologically proved hypertrophic pyloric stenosis gastric juice analyses were performed according to Lambling. Basic acid output and maximal acid output in these infants were significantly increased as compared to healthy infants of the same age group. The higher acid output in the hypertrophic pyloric stenosis group was due to higher volumes and a higher acidity of the gastric juices. Basic acid output and maximal acid output increased following pylorotomy. There is evidence, that hyperacidity in pylorus stenosis of infancy is primarily and not due to the pyloric constriction. There was a distinct correlation between the degree of metabolic alkalosis and diminished acid outputs. The findings support the thesis, that infantile hypertrophic stenosis is originated by an increased parietal cell mass. The increased acid secretion and the enhanced release of secretin and cholecystokinin are supposed to originate the hypertrophy of the pyloric muscle.
 ...
PMID:[Results of Lambling gastric juice analysis in infants with spastic hypertrophic pyloric stenosis (SHPS)]. 373 14

Caerulein was shown to delay gastric emptying in conscious rats in a dose-dependent fashion. The threshold dose was about 0.05 mug/kg by the intraperitoneal route. Maximum effect was obtained with 5 mug/kg. Neutralization of acidity or reduction of gastric juice by mean of NaHCO3 or cimetidine, respectively, did not modify the effect of the peptide. Chlorpheniramine was similarly ineffective. The effect of caerulein on gastric emptying was most probably connected with a strong contraction of the gastroduodenal junction previously observed in different experimental conditions and was not affected by H1- or H2-histamine antagonists. The C-terminal heptapeptide of cholecystokinin behaved quite similarly to caerulein. The present study emphasizes the close parallelism between results obtained in the in situ stomach preparation of anaesthetized rats and gastric emptying in conscious animals.
 ...
PMID:Action of caerulein on gastric emptying of the conscious rat. 743 33

Helicobacter pylori infection may be associated with duodenal ulcer (DU) and accompanied by enhanced gastrin release but the mechanism of this H pylori related hypergastrinaemia in DU patients is unclear. Cholecystokinin (CCK) has been implicated in the feedback control of gastrin release and gastric acid secretion in healthy subjects. This study therefore investigated if CCK participates in the impairment of postprandial gastrin release and gastric secretion in six DU patients. Tests were undertaken with and without elimination of endogenous CCK by loxiglumide, a selective CCK-A receptors antagonist, before and after eradication of H pylori with triple therapy (omeprazole, amoxicyllin, bismuth). In H pylori positive DU patients, the post-prandial decline in pH (with median pH 3.5) was accompanied by a pronounced increment in plasma gastrin but the administration of loxiglumide did not affect significantly this postprandial rise in plasma gastrin and gastric pH profile. After eradication of H pylori, the plasma gastrin concentration was reduced while the median postprandial pH was significantly increased (median pH 4.3). The administration of loxiglumide resulted in significantly greater increase in postprandial plasma gastrin and greater decrease in pH (median pH 3.1) in these patients. This study shows that (a) infection with H pylori is accompanied by an enhanced gastrin release and gastric acidity in DU patients, (b) the failure of loxiglumide to affect plasma gastrin or gastric acid secretion in H pylori infected DU patients could be attributed, at least in part, to the failure of endogenous CCK to control gastrin release and gastric secretion by releasing somatostatin, and (c) the test with loxiglumide may be useful in the identification of patients with impaired feedback control of gastrin release and gastric secretion resulting from infection with H pylori.
 ...
PMID:Eradication of Helicobacter pylori restores the inhibitory effect of cholecystokinin on postprandial gastrin release in duodenal ulcer patients. 748 32

CCK8 is a poor stimulant of gastric acid secretion in vivo, but is equipotent to gastrin-17 (G17) in in vitro systems. To further evaluate the role of cholecystokinin (CCK) in regulating acid output in humans, dose-response curves were constructed to CCK8 or G17 (6.4-800 pmol kg-1 per h) with and without a specific CCK-A receptor antagonist (loxiglumide). During loxiglumide infusion, G17-stimulated acid output was unchanged, whereas CCK8-stimulated secretion increased significantly. Gastric somatostatin-14 release increased fivefold with CCK8 alone, but was blocked with loxiglumide administration. These data suggest that CCK8 directly stimulates acid secretion by binding to a CCK-B/gastrin receptor on parietal cells, but at the same time inhibits acid responses by stimulating gastric somatostatin release to a CCK-A receptor-mediated pathway. To test which action of CCK is relevant under physiological circumstances, the effect of loxiglumide on fasting and post-prandial acidity was measured through continuous pH-metry. After eating, gastrin levels increased fourfold compared to controls with concomitant increases in acid secretion. These results suggest that post cibum, CCK is an inhibitor of acid secretion by regulating gastrin through local somatostatin; they support the hypothesis that CCK acts as an enterogastrone.
 ...
PMID:Cholecystokinin is a physiological regulator of gastric acid secretion in man. 795 87

Gastric acid secretion in response to pylorus-ligation and duodenal fat feeding in Otsuka Long-Evans Tokushima Fatty (OLETF) rats without cholecystokinin-A receptor was examined. Acidity of gastric juice obtained from pylorus-ligated OLETF rats was significantly lower than that of control LETO rats. Gastric acid secretion in response to bethanechol, pentagastrin, or atropine was maintained in both OLETF and LETO rats. Intraduodenal lipid injection strongly inhibited gastric acid secretion in control LETO rats. In contrast, administration of lipid into the duodenum failed to inhibit acid secretion in OLETF rats. These results suggest that basal gastric acid secretion may be impaired in OLETF rats and that the cholecystokinin-A receptor is involved in lipid-induced acid inhibition.
 ...
PMID:Intraduodenal lipid does not inhibit acid secretion in OLETF rats not expressing CCK-A receptor gene. 894 69


1 2 Next >>