• Journal of Pharmaceutical Investigation
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• v.19 no.4
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• pp.185-190
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• 1989

The release of angiotensin and ${\alpha}-amylase$ from monolithic devices of different molecular weight of polyethylene glycol (PEC) grafted polyurethane copolymer was investigated. Water-soluble PEG grafted polymer provided a controlled release of angiotensin and ${\alpha}-amylase$. The release rate of angiotensin and ${\alpha}-amylase$ could be controlled by varying the molecular weight of PEC grafted. The release mechanism may be associated with the creation of pore or domain through the devices following the gel swelling and self-aggregation by PEC grafted polymer. Hydrophobic polyurethane grafted with PEG can provide a biomaterial for prolonged release of angiotensin and ${\alpha}-amylase$ from angiotensin and ${\alpha}-amylase$ blended system.

• International Journal of Oral Biology
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• v.31 no.4
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• pp.127-133
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• 2006

[ $H_2O_2$ ], a member of reactive oxygen species (ROS), is known to be involved in the mediation of physiological functions in a variety of cell types. However, little has been known about the physiological role of $H_2O_2$ in exocrine cells. Therefore, in the present study, the effect of $H_2O_2$ on cholecystokinin (CCK)-evoked $Ca^{2+}$ mobilization and amylase release was investigated in rat pancreatic acinar cells. Stimulation of the acinar cells with sulfated octapeptide form of CCK (CCK-8S) induced biphasic increase in amylase release. Addition of $30\;{\mu}M\;H_2O_2$ enhanced amylase release caused by 10 pM CCK-8S, but inhibited the amylase release induced by CCK-8S at concentrations higher than 100 pM. An ROS scavenger, $10\;{\mu}M$ Mn(III)tetrakis(4-benzoic acid)porphyrin chloride, increased amylase release caused by CCK-8S at concentrations higher than 100 pM, although lower concentrations of CCK-8S-induced amylase release was not affected. To examine whether the effect of $H_2O_2$ on CCK-8S-induced amylase release was exerted via modulation of intracellular $Ca^{2+}$ signaling, we measured the changes in intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in fura-2 loaded acinar cells. Although $30\;{\mu}M\;H_2O_2$ did not induce any increase in $[Ca^{2+}]_i$ by itself, it increased the frequency and amplitude of $[Ca^{2+}]_i$ oscillations caused by 10 pM CCK-8S. However, $30\;{\mu}M\;H_2O_2$ had little effect on 1 nM CCK-8S-induced increase in $[Ca^{2+}]_i$. ROS scavenger, 1 mM N-acetylcysteine, did not affect $[Ca^{2+}]_i$ changes induced by 10 pM or 1 nM CCK-8S. Therefore, it was concluded that $30\;{\mu}M\;H_2O_2$ enhanced low concentration of CCK-8S-induced amylase release probably by increasing $[Ca^{2+}]_i$ oscillations while it inhibited high concentration of CCK-8S-induced amylase release.

• The Korean Journal of Pharmacology
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• v.17 no.2
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• pp.31-36
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• 1981

Heavy metals which are present as trace elements in human body have been known to modify various enzymatic reaction. These metals can be essential or non-essential. Zinc, copper and calcium are essential in maintaining some biological processes, whereas non-essential metals such as cadmium, lead and mercury produce accumulatve toxic effect. Cadmium accumulated in pancreas can cause toxicity and damage of pancreatic cells, thereby influencing CHO metabolism. Lead compounds are known to produce toxic effects on the kidney, digestive system and brain fellowed by inhibition of activity of ${\rho}-aminolevulinic$ acid and biosynthesis of hemoproteins and cytochrome. Evidence has been accumulated that zinc not only acts as a cofactor in enzyme reaction but also prevents toxic effect induced by heavy metal such as copper and cadmium. To demonstrate the effect of heavy metals on pancreatic secretion, part of uncinate pancreas was taken and incubated in Krebs-Ringer bicarbonate buffer with heavy metals used. Additional treatment with CCK-OP was performed when needed. After incubation during different period of time, medium was analyzed for amylase activity using Bernfeld's method. The present study was attempted in order to elucidate the effect of several kinds of heavy metal on exocrine pancreatic secretion in vitro. The results obtained are as follows: 1) CCK-OP stimulated significantly amylase release from pancreatic fragments in vitro. 2) CCK-OP response of amylase release from pancreatic fragments was inhibited by treatmant with cadmium, especially high doses of cadmium. 3) CCK-OP response of amylase release from pancreatic fragments was inhibited when pretreated with $10^{-4}M$ copper chloride. 4) Lead chloride at the concentration of $10^{-3}M\;and\;10^{4}M$ stimulated the basal amylase release in vitro but CCK-OP response did not augment by lead chloride. 5) Zine chloride did not affect amylase release from pancreatic fragment in vitro. From the results mentioned above, it is suggested that CCK-OP response was inhibited it the amylase release from pancreatic fragments pretreated with cadmium and copper chloride.

• Asian-Australasian Journal of Animal Sciences
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• v.2 no.3
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• pp.187-188
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• 1989

• The Korean Journal of Pharmacology
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• v.19 no.1
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• pp.71-76
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• 1983

Aminoglycoside antibiotics are reported to enhance the amylase release from isolated slices of pancreas in vitro and the mode of action of aminoglycosides on amylase release is considered different from those of acetylcholine or cholecystokinin(CCK), i.e., electronmicroscopically intact zymogen granules are appeared in the lumen of pancreatic acini by treatment of aminoglycosides. It is known that atropine blocks the secretagogue effect of acetylcholine, and phenoxybenzamine is reported to block the effects of CCK or its analogue caerulein. Present study was undertaken to investigate the mode of action of aminoglycosides on the amylase release using atropine, phenoxybenzamine and propranolol as a membrane stabilizing agent in slices of chicken pancreas. The results are summarized as follows : 1) Streptomycin and kanamycin increased the amylase release significantly from slices of chicken pancreas. 2) The effect of streptomycin was inhibited by atropine but not by phenoxybenzamine or propranolol. 3) The amylase release by acetylcholine was blocked by atropine tut the effect of cholecystokinin octapeptide(CCK-8) was not influenced by atropine, phenoxybenzamine or propranolol. 4) Pretreatment of streptomycin enhanced the secretagogue effect of acetylcholine or CCK-8. From these results it is suggested that amylase releasing effects of aminoglycosides are mediated in part by cholinergic stimulation and in part by membrane alteration and these effects are enhanced by acetylcholine or cholecystokinin.

• Asian-Australasian Journal of Animal Sciences
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• v.2 no.3
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• pp.193-194
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• 1989

• The Korean Journal of Physiology
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• v.29 no.2
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• pp.243-250
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• 1995

A possible potentiation between cholecystokinin (CCK) and secretin in amylase secretion from isolated rat pancreatic acini was investigated. Combined treatment of acini with secretin and CCK at low concentrations, which are known to be physiological, resulted in enzyme secretion larger than the arithmetic sum of their separate effects. Such a potentiating effect also occurred between secretin and A23187 (Ca ionophore), between forskolin (adenylate cyclase activator) and CCK, and between forskolin and A23187. Staurosporin (protein kinase C inhibitor) and W7 (calmodulin antagonist) inhibited markedly the potentiated amylase release induced by the agonists, but KT5720 (protein kinase A inhibitor) did not affect the potentiated amylase release. Therefore, we concluded that the action of CCK in a physiological concentration is potentiated by secretin in a physiological concentration range and vice versa, and that the intracellular mechanism necessary for the potentiation is associated with $Ca^{2+}$. However, it is uncertain what mechanisms are involved in potentiation of amylase release after CAMP and $Ca^{2+}$.

• The Korean Journal of Pharmacology
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• v.30 no.2
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• pp.205-215
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• 1994

It is well known that chronic stimulation with CCK gives rise to growth of exocrine pancreas and to increased content of enzyme proteins in pancreas. However, littls Is known about changes of the secretory function of exocrine pancreas which has been chronically stimulated with CCK, especially about the responsiveness to secretagogues such as CCK, caerulein and carbachol. The present study was performed to investigate the effect of camostat on secretory profiles and the responsiveness to secretagogues of exocrine pancreas by observing in vitro amylase release stimulated by cholecystokinin-octapeptide(CCK-8) and carbachol in dispersed isolated pancreatic acini from camostat-treated rats for 4 or 10 days. The results summarized as follows : 1) The maximal effective concentration of CCK-8 in amylase release in the camostat treated group was greater than control group, but that of carbachol was not different between groups. 2) Analysis of the stimulated amylase release as the percentage of the maximal response revealed that camostat treatment caused right-shift of the dose-response curve of CCK-8. Camostat did not cause significant changes in the dose-response curve of carbachol. 3) There were considerable increases in the amylase release in the camostat-treated group, compared to the control when acini were stimulated with CCK-8 $10^{-9}\;M$ and carbaochol $10^{-6}\;M$, and higher concentrations. 4) There was a reverse correlation between the tissue content and the maximal release(percent of the total content) of amylase. These results suggest that chronic exposure of exocrine pancreas to increased endogenous CCK can enhance the responsiveness of exocrine enzyme secretion to secretagogues, especially at higher concentrations of CCK and carbachol.

• Microbiology and Biotechnology Letters
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• v.13 no.4
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• pp.403-408
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• 1985

Enhancement of surfactant on release of secretory enzyme, such as $\alpha$-amylase, acid phosphatase and alkaline phosphatase, was investigated during submerged culture of Rhizopus oryzae. Morphological changes of colony was occured; small pelletal form in 0.18mM of sodium dodecyl sulfate, pulpy form in 0.48mM of sodium deoxycholate, and filamentous form in absence of surfactant. It. Supplement of sodium dodecyl sulfate induced 9 times increasing activity of $\alpha$-amylase and that of acid phosphatase 25 times in cultural fluids. Alkaline phosphatase was increased 11 times in cultural fluid and also stimulated in cytoplasm with supplement of sodium deoxycholate.

• The Korean Journal of Pharmacology
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• v.20 no.2
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• pp.49-57
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• 1984

The exocrine pancreatic secretion is controlled mainly by gastrointestinal hormones as well as cholinergic nerves. The adrenergic influence on exocrine pancreas is thought not to he important and the evidences supporting this contention are still contradictory. In an effort to elucidate the adrenergic influence on the exocrine pancreas, we have determined the amylase release from pancreatic slices of rats treated with adrenergic drugs. The albino rats of either sex, weighing $60{\sim}80\;g$, were decapitated and the uncinate pancreata were isolated and incubated in screw top vials containing 2 ml krebs-Ringer bicarbonate buffer solution gassed with 95% $O_2$ and 5% $CO_2$. These vials were shaken continuously in a waterbath maintained at $37^{circ}C$, and enzyme release was stimulated with acetylcholine$(10^{-5}M)$. For chronic treatment methoxamine$(an\;{\alpha}-adrenergic\;agonist,\;5\;mg/kg)$, isoproterenol (a\;{\beta}-adrenergic\;agonist,\;10\;mg/kg) and reserpine (0.5 mg/kg) along with cholecystokinin octapeptide$(CCK-op,\;2{\mu}g/kg)$ were given i.p. in rats daily for 3, 5, 7, 9 or 12 days. For acute experiment these drugs were added directly to the incubation medium in a concentration of $10^{-5}M$ except CCK-OP $(10^{-9}M)$. The results are summarized as follows. 1) The addition of methoxamine, isoproterenol or reserpine to the incubation medium containing pancreatic slices augmented the release of amylase induced by acetylcholine and among them the effect of isoproterenol was most prominent. 2) Chronic treatment of methoxamine or reserpine caused enhancement of acetylcholine response in amylase release from pancreatic slice throughout the experimental period, but the amylase release was less than that of control by 12 days isoproterenol treatment. 3) In the pancreatic slices obtained from 12 days treatment of CCK-OP, the amylae release responding to acetylcholine was enhanced. By these finding it is suggested that methoxamine, isoproterenol and reserpine had marked influence on the exocrine pancreatic functions in rats and that these effects are due to their inherent actions rather than sympathetic nerve or adrenergic receptor function.