Disease relevance of pentagastrin

• Starting in 1975, we screened 300 subjects in four large families with MEN-2A for expression of the disease, using measurements of plasma calcitonin after stimulation with pentagastrin or calcium and urinary excretion of catecholamines and catecholamine metabolites [1].
• The carcinoid flush. Provocation by pentagastrin and inhibition by somatostatin [2].
• In an unselected group of patients with pheochromocytoma, we performed pentagastrin tests, parathyroid hormone assays, computed tomography (CT) or magnetic resonance imaging (MRI) of the brain, ophthalmoscopy, CT imaging of the abdomen, and ultrasonography of the testes [3].
• Atrial fibrillation after administration of calcium and pentagastrin [4].
• Increased sensitivity to stimulation of acid secretion by pentagastrin in duodenal ulcer [5].

Psychiatry related information on pentagastrin

• When colonic motor activity was increased with cholecystokinin or pentagastrin, patients with irritable bowel syndrome showed a marked increase in 3-cycle per min contractile activity, occurring simultaneously with 3-cycle per min slow wave activity [6].
• CONCLUSIONS: In response to central vagal stimulation with RX 77368, gastric defense mechanisms were enhanced through prostaglandin-dependent and -independent pathways, in contrast to the prostaglandin-independent effects of intravenous pentagastrin [7].
• CONCLUSIONS: Patients with generalized anxiety disorder appear to exhibit greater subjective sensitivity to pentagastrin than do normal subjects [8].
• Pentagastrin-induced sleep panic attacks: panic in the absence of elevated baseline arousal [9].
• Anxiogenic effects of pentagastrin in patients with social phobia and healthy controls [10].

High impact information on pentagastrin

• Growth hormone secretion and pentagastrin [11].
• To detect familial medullary thyroid carcinoma in a premetastatic stage, we administered tests provocative of calcitonin secretion (infusion of calcium or pentagastrin or both) each year for seven years to members of a pedigree now numbering 107 [12].
• However, in the 2-week-old rat neither exogenous histamine nor the H-2 receptor agonist impromidine stimulates acid secretion, whereas pentagastrin and the cholinergic agent bethanechol are potent stimuli [13].
• Intrahypothalamic injections of 100 picomoles of pentagastrin or natural gastrin promptly increased secretion of gastric acid in conscious rats [14].
• We studied acid secretory responses to exogenous pentagastrin and to exogenous and endogenous gastrin in 12 stable cirrhotic subjects with portacaval shunt, 12 unshunted cirrhotics, and 12 normal subjects [15].

Chemical compound and disease context of pentagastrin

• Fundic mucosal excision abolished the mean response of the gastric fistula and reduced its maximal response to pentagastrin and to histamine by 85% [16].
• The relationship between the stimulation state of the parietal cells and the gastric antisecretory properties of omeprazole has been evaluated in dogs with gastric fistulas maximally stimulated with pentagastrin [17].
• Nude mice bearing xenografts of colon cancer CX1 or X56 were treated for 14-25 days subcutaneously with saline, pentagastrin (0.5 or 1.0 mg/kg), proglumide (250 or 500 mg/kg), or somatostatin 14 (33, 100, or 300 micrograms/kg) twice daily [18].
• Effect of bethanechol (urecholine) on gastric acid and nonparietal secretion in normal subjects and duodenal ulcer patients. Comparison with atropine, pentagastrin, and histamine [19].
• The sphincter response to both edrophonium and pentagastrin after esophagitis was induced was significantly less than preperfusion responses [20].

Biological context of pentagastrin

• By contrast, although both pentagastrin and heptadecapeptide gastrin inhibited gastric emptying, the doses required for this action were much higher than the D50's required for stimulation of gastric acid secretion [21].
• Pentagastrin has no influence on cell proliferation in fed rats [22].
• Fundic distention with a baloon volume eliciting a maximal acid response to distention either left unchanged or suppressed the maximal acid secretory rate produced by pentagastrin in 7 nonoperated and 6 vagotomized DU patients and in 5 healthy subjects [23].
• Pentagastrin increased acid secretion, oxygen consumption, and both total and mucosal blood flow [24].
• Pentagastrin induced a 2.3-fold increase in the parietal cell volume density in the regenerating mucosa and a 1.3-fold increase in normal mucosa [25].

Anatomical context of pentagastrin

• The effects of pentagastrin on lower esophageal sphincter (LES) pressure has been studied in trained, unanesthetized dogs [26].
• CRF microinjected into the third cerebral ventricle decreased pentagastrin-stimulated gastric acid secretion for 3 h (P less than 0.01) dose-dependently (0.2-6.0 nmol X kg-1) [27].
• This is the first case to be reported in which the heterotopic mucosa was actually shown to secrete measurable acid in response to pentagastrin [28].
• Histamine metabolism in human gastric mucosa. Effect of pentagastrin stimulation [29].
• Pentagastrin had no effect on weight, deoxyribonucleic acid synthesis, or deoxyribonucleic acid content of oxyntic gland area, duodenum, or colon [30].

Associations of pentagastrin with other chemical compounds

• This same dose of PYY maximally inhibited histamine- and pentagastrin-stimulated acid secretion by 28 +/- 7% (P less than 0.05), and 17 +/- 4% (P less than 0.05), respectively [31].
• The gastric inhibitory action of intracerebroventricularly administered CRF on pentagastrin-stimulated gastric acid secretion was completely abolished by ganglionic blockade with chlorisondamine [27].
• Morphologically typical ulcers were produced in the first part of the duodenum in 300 male Wistar rats by subcutaneous infusion for 24 hr of pentagastrin (4 mug per kg-min) and carbachol (0.8 mug per kg-min) [32].
• Ninety minutes after mucosal exposure to 2 M NaCl there was an almost complete restitution of the gastric surface epithelium in pentagastrin-stimulated and cimetidine-treated animals, whereas about 15% of the gastric surface still showed damage in animals in which acid secretion was not interfered with [33].
• CONCLUSIONS: The significantly higher gland luminal pressure after treatment with omeprazole, compared with the values during pentagastrin or vehicle infusion, cannot be explained by increased mucus thickness [34].

Gene context of pentagastrin

• Somatostatin 14 or the sst2 agonist DC 32-87 inhibited pentagastrin-stimulated acid secretion in wild-type mice, but did not alter basal secretion in knockout mice [35].
• The intracerebroventricular administration of the nonselective CCK receptor agonist caerulein or the selective CCK-B receptor agonist pentagastrin increased dose dependently the level of anxiety [36].
• Pentagastrin provides a readily available alternative to CCK4 for studying the CCK receptor system and exploring its involvement in human anxiety [37].
• We utilized intravenous infusions of pentagastrin, a selective CCK-B receptor agonist, and studied behavioral and cardiovascular responses in 10 patients with panic disorder and 10 normal controls [37].
• CCK sulphated octapeptide (1-10 microM), but not pentagastrin or CCK unsulphated octapeptide, was found to cause a dose-dependent increase in the release from the posterior nucleus accumbens [38].

Analytical, diagnostic and therapeutic context of pentagastrin

• By parallel line bioassay non-DU subjects required 2.8 times more pentagastrin (95% confidence limits 2.1-3.7) than DU highest response [5].
• Intravenous infusion of pentagastrin (0.1--0.4 microgram/kg/min) resulted in an increase in acid output in desalivated rats although the responses was less than that observed in sham-operated controls [39].
• After bilateral transthoracic vagotomy, pentagastrin infusion still interrupted the complex but now, in addition, upon stopping the pentagastrin, a premature activity front (phase III) of the complex was also followed by a reduction in the temporal regularity of the cycles of the complex [40].
• Inclusion of pentagastrin in the perfusion buffer increased acid output from 2.2 +/- 0.4 microEq H+/h during control perfusion to 18.8 +/- 1.8 microEq H+/h (p less than 0.01) [41].
• In 8 nonoperated DU subjects and in 5 DU patients subjected to proximal gastric vagotomy, low grade fundic distention moderately enhanced the acid output evoked by a threshold dose of pentagastrin [23].

References