The effect of diazepam on human pancreatic secretion.
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The effect of intravenous and intramuscular administration of diazepam on secretin- and cholecystokinin-stimulated pancreatic secretion was studied in man. Diazepam was not found to have a significant effect on mean volume out-put, bicarbonate and enzyme concentrations and colour index. It was acceptable as premedication for routine pancreatic function studies.Keywords:
Premedication
Secretin
Pancreatic function
Pancreatic enzymes
Bicarbonate
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Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates protein and/or amylase secretion from isolated rat pancreatic acini. The effect of PACAP on pancreatic secretion in vivo and its mechanism of action were studied.Rats were prepared with pancreatic duct cannulation, pyloric ligation, and bile diversion into duodenum, and 2.5, 5, and 10 nmol/kg PACAP-27 was administered intravenously while pancreatic juice was collected for 30 minutes. In other groups of rats, the effect of 10 nmol/kg PACAP-27 was studied under the influence of either atropine; loxiglumide, an antisecretin serum; a combination of both loxiglumide and the antiserum; or a PACAP antagonist (PACAP 6-38). Plasma secretin and cholecystokinin concentrations were measured by radioimmunoassay.(1) PACAP dose-dependently increased pancreatic secretion of fluid, bicarbonate, and protein; (2) the increase in pancreatic secretion paralleled that of plasma secretin and cholecystokinin; (3) a combination of loxiglumide and antisecretin serum eliminated the PACAP-stimulated pancreatic secretion, whereas loxiglumide or antisecretin serum alone partially but significantly blocked pancreatic secretion; (4) atropine failed to influence PACAP-induced pancreatic secretion; and (5) PACAP antagonist profoundly suppressed the PACAP action.PACAP-27 dose-dependently stimulates pancreatic secretion of fluid, bicarbonate, and protein in rats. This effect is mediated by release of both secretin and cholecystokinin and is independent of cholinergic tone.
Secretin
Proglumide
Gastrointestinal hormone
Pancreatic juice
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The effect of intravenous and intramuscular administration of diazepam on secretin- and cholecystokinin-stimulated pancreatic secretion was studied in man. Diazepam was not found to have a significant effect on mean volume out-put, bicarbonate and enzyme concentrations and colour index. It was acceptable as premedication for routine pancreatic function studies.
Premedication
Secretin
Pancreatic function
Pancreatic enzymes
Bicarbonate
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The effects of gastrointestinal hormones on cAMP accumulation and parathyroid hormone (PTH) release were investigated in dispersed bovine parathyroid cells. Secretin (10 (-7) M) caused a 4- to 6-fold increase in cAMP accumulation, while glucagon, vasoactive intestinal peptide, and gastrin caused little if any stimulation. Cholecystokinin caused a 2- to 3-fold increase in cAMP accumulation at 10(-6) M, but this effect may be related to contamination with endogenous secretin since synthetic cholecystokinin octapeptide had no effect. Maximal intracellular cAMP accumulation due to 10(-7) M secretin was reached within 5 min and returned to control over the next 30-60 min, concomitant with a progressive rise in extracellular cyclic nucleotide. cAMP accumulation was half-maximally stimulated by 5 x 10(-9) to 1 x 10(-8) M secretin and was unaffected by alpha- or beta-adrenergic or dopaminergic blockers. Parallel effects were noted on PTH release : 10(-8) M secretin caused a 20-50% increment in PTH release at 15 min which persisted for up to 2 h; PTH release was stimulated half-maximally by approximately 6--8 x 10(-9) m secretin. The specificity of the observed results for secretin and the lack of effect of adrenergic antagonists suggest the presence of a receptor for secretin on dispersed bovine parathyroid cells. These results also suggest the possibility that secretin may modulate parathyroid function in vivo in the cow.
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Secretin family
Gastrointestinal hormone
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Pancreatic Secretion of Zinc and Copper in Normal Subjects and in Patients with Chronic Pancreatitis
Pancreatic secretion of zinc and copper in duodenal juice were measured in 7 healthy persons and in 9 patients with chronic pancreatitis. Stimulation with cholecystokinin and secretin increased secretion of zinc in healthy persons but not in patients. Copper secretion was not influenced. In patients with chronic pancreatitis, the correlations between zinc secretion, and amylase and trypsin secretion were significant while in healthy subjects they were not. Possibly pancreatic zinc secretion in the duodenal juice might be used as a measure of exogenic pancreatic function, and determination of zinc in duodenal juice may replace enzyme determinations in the diagnosis of chronic pancreatitis.
Secretin
Pancreatic function
Pancreatic juice
Pancreatic enzymes
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The influence of the endocrine pancreas on exocrine pancreatic function was studied in rats made diabetic by administration of streptozotocin. In normal urethan-anesthetized rats the C-terminal octapeptide of cholecystokinin (CCK-8) stimulated the rate of flow and rates of amylase and trypsinogen release from the pancreas; the proportions of the two enzymes did not change with repeated stimulation. In diabetic rats CCK-8 (0.3-1.2 nmol . kg-1 iv) stimulated significantly greater increases in trypsinogen output and rate of flow compared with normal animals. In contrast, amylase responses to CCK-8 were significantly depressed in diabetic rats. There were no differences between normal and diabetic rats in the flow and total protein responses to exogenous secretin. The present results indicate that the effects of insulin deprivation on relative rates of enzyme synthesis are also expressed in the secretion of the intact pancreas in vivo. These results also raise the possibility that in the normal intact gland there may be nonparallel release of enzymes at different rates of secretion depending on the relative secretory activities of cells in the immediate vicinity of the islets of Langerhans and those distant to the islets.
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Chymotrypsinogen
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Concentrations of cholecystokinin (CCK) and secretin from neonatal guinea pig plasma were evaluated in relation to pancreatic growth, and secretion from dispersed pancreatic acini. Plasma CCK was low at birth (3.1 +/- 0.8 pmol/L) but rose markedly by day 15 (11.0 +/- 0.8 pmol/L, p < 0.001). Plasma secretin was also low at birth (3.8 +/- 0.8 pmol/L) but peaked on day 4 (17.0 +/- 1.4 pmol/L, p < 0.001) and remained elevated through d 15. Adult nonfasting plasma CCK and secretin levels were 12.3 +/- 0.8 and 8.9 +/- 1.5 pmol/L, respectively. Pancreatic weight more than doubled during the first week of life, with the greatest increase during the first 4 d (156 +/- 4 to 262 +/- 10 mg/100g body wt, p < 0.001). Body weight increased most dramatically during the second week (126 +/- 9 to 190 +/- 7 g p < 0.001). Amylase secretion from isolated acini stimulated by CCK-8, carbachol, phorbol ester, forskolin, and calcium ionophore (A23187) was present at birth. The percentage of total amylase content secreted in response to CCK, carbamylcholine, and secretin did not change during the first 2 wk of neonatal life, and was independent of surges in circulating CCK and secretin. These results indicate that functional maturity of the guinea pig pancreas for amylase secretion occurs early and is different from the rat, mouse, pig, and human. Since results can readily be compared between animals of different postnatal ages, the neonatal guinea pig is ideally suited for the study of hormonal effects on acinar cell function.
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Gastrointestinal hormone
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The effect of gastrin-releasing peptide (GRP) (250, 500, 1000 pmol/kg.h) on the pancreaticobiliary bicarbonate secretion, the pancreatic protein secretion, and the plasma concentrations of secretin and cholecystokinin (CCK) was studied in the anaesthetized pig. Infusion of GRP (1000 pmol/kg.h) increased the portal plasma concentrations of secretin from 0.9 to 13.6 pmol/l and CCK from 1.2 to 38.4 pmol/l, the pancreatic bicarbonate secretion from 0.01 to 5.6 mmol/h, the hepatic bicarbonate secretion from 0.5 to 4.1 mmol/h, and the pancreatic protein secretion from 3 to 680 mg/h. Blocking of CCK-A receptors by MK-329 did not significantly change the effect of GRP, whereas prevention of secretin release by removal of the small intestine caused a 13-fold reduction in the GRP-induced pancreatic bicarbonate secretion and completely abolished the effect on hepatic bicarbonate secretion but did not change the effect on pancreatic protein secretion. We conclude that the effect of GRP on pancreaticobiliary bicarbonate secretion is not mediated through the release of CCK but more likely through the release of secretin and that the effect on pancreatic protein secretion is possibly a direct effect of GRP.
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Bicarbonate
Gastrin-releasing peptide
Gastrointestinal hormone
Secretin family
Pancreatic juice
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Pure porcine cholecystokinin-33 [the triacontatriapeptide form of cholecystokinin (CCK-33)], gastric inhibitory polypeptide (GIP), and secretin were infused in rats in doses of 1, 10, and 100 pmol/kg·min. The pep tides were administered alone or in combination with glucose (40 mg/kg·min) or arginine (50 mg/kg·min). In the basal state, CCK-33 and GIP produced significant hypoglycemia at all concentrations used, although they elevated insulin levels only at the highest dose. Secretin had no effect. CCK-33 at a dose of 1 pmol/kg·min enhanced the secretion of insulin induced by glucose or arginine. These effects were more pronounced when higher doses of CCK-33 were administered. GIP at a dose of 1 pmol/kg·min had no effect on insulin release. Higher doses of GIP significantly potentiated insulin release stimulated by glucose or arginine. Secretin (100 pmol/kg·min) had no clear-cut effect on glucose-induced insulin secretion, but it slightly enhanced arginine-induced secretion. All hormones investigated, at all doses used, significantly stimulated the arginine-induced secretion of glucagon. We conclude that CCK-33 is a potent stimulatory factor of glucose-and arginine-induced insulin secretion and should therefore be taken into consideration as an incretin candidate. In addition, CCK-33 and GIP modulate glucose homeostasis by affecting glucagon release.
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Gastric inhibitory polypeptide
Secretin family
Pancreatic polypeptide
Gastrointestinal hormone
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The effect of intravenous injection of secretin and cholecystokinin-pancreozymin (C-P) on serum immunoreactive insulin (IRI) in monkeys and rats was measured. Both secretin (7.5 U) and C-P (30 U) injections caused 4- to 5-fold increases in serum IRI of monkeys within 2 min. Only C-P (2 U) injections caused an increase (about 4-fold) in serum IRI of rats, while after secretin (0.5 U) injections there was no change in IRI. The serum glucose decreased in the monkeys following the increased IRI, but in neither species did serum glucose increase and therefore glucose was not the cause of the IRI response. In a separate experiment it was shown that neither secretin nor C-P increases appreciably the glucose uptake of isolated fat cells from epididymal fat pads of rats. (Endocrinology86: 927, 1970)
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Gastric inhibitory polypeptide
Secretin
Gastrointestinal hormone
Secretin family
Pancreatic polypeptide
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Citations (35)