• The Korean Journal of Physiology and Pharmacology
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• v.6 no.2
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• pp.87-91
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• 2002

The aim of this study was to investigate the role of $Ca^{2+}-channel$ blockers in norepinephrine (NE) release from rat hippocampus. Slices and synaptosomes were incubated with $[^3H]-NE$ and the releases of the labelled products were evoked by 25 mM KCl stimulation. Nifedipine, diltiazem, nicardipine, flunarizine and pimozide did not affect the evoked and basal release of NE in the slice. But, diltiazem, nicardipine and flunarizine decreased the evoked NE release with a dose-related manner without any change of the basal release from synaptosomes. Also, a large dose of pimozide produced modest decrement of NE release. ${\omega}-conotoxin$ (CTx) GVIA decreased the evoked NE release in a dose-dependent manner without changing the basal release. And ${\omega}-CTxMVIIC$ decreased the evoked NE release in the synaoptosomes without any effect in the slice, but the effect of decrement was far less than that of ${\omega}-CTxGVIA.$ In interaction experiments with ${\omega}-CTxGVIA,\;{\omega}-CTxMVIIC$ slightly potentiated the effect of ${\omega}-CTxGVIA$ on NE release in the slice and synaptosomal preparations. These results suggest that the NE release in the rat hippocampus is mediated mainly by N-type $Ca^{2+}-channels,$ and that other types such as L-, T- and/or P/Q-type $Ca^{2+}-channels$ could also be participate in this process.

• YAKHAK HOEJI
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• v.45 no.3
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• pp.282-286
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• 2001

To investigate the different mechanism between ATP and compound 48/80 (C$_{48}$80/)-induced histamine release, we observed effects of calcium antagonists in histamine release of rat peritoneal mast cells. Verapamil and diltiazem (voltage-dependent calcium channel blocker) and TMB-8 (a blocker of intracellular calcium release) significantly inhibited ATP-induced histamine release, but did not inhibit $C_{48}$80/-induced histamine release. Econazole (a blocker of receptor-operated calcium channel) dose-dependently inhibited both ATP and $C_{48}$80/-induced histamine release, but inhibitory effect of econazole in ATP-induced histamine release was more potent than that in $C_{48}$80/-induced histamine. EGTA dose-dependently inhibited ATP and $C_{48}$80/-induced histamine release, but $C_{48}$80/-induced histamine release was slightly inhibited by high concentrations (>2 mM) of EGTA. These results suggest that ATP-induced histamine release is related to broth intracellular calcium release and extracellular calcium influx via voltage-dependent calcium channel and receptor-operated calcium channel. $C_{48}$80/-induced histamine release is related to extracellular calcium influx, especially by receptor-operated calcium channel rather than voltage-dependent calcium channel.

• Toxicological Research
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• v.14 no.3
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• pp.349-356
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• 1998

We identified S9940, a novel microbial metabolite from Streptomyces spp., to inhibit the release of neurotransmitter from PC12 cells. S9940 is an inhibitor of trifiated norepinephrine ([$^{3}H$]-NE) release in high $K^+$ buffer solution containing ionomycin, indicating that S9940 inhibits neurotransmitter release after the influx of $Ca^{2+}$ ions. We also examined the effect of S9940 on $\beta-glucuronidase$ release from guinea pig neurophils and the effect on the neurite extension of PC12 cells and rat hippocampal neurons. As a result, S9940 inhibited $\beta-glucuronidase$ release: when treated with $5{\mu}g/ml$ of S9940, which prevented [$^{3}H$]-NE release, the inhibition of neurite extension for both PC12 cells and rat hippocampal neurons was observed.

• Korean Journal of Veterinary Research
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• v.48 no.1
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• pp.27-32
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• 2008

The present study was carried out to develop a sustained release implantable formula of bovine somatotropin (SRIF-BST) and to examine its sustained release effect. The SRIF-BST was produced by coating a solid pellet, which was comprised of BST and an excipient, made of a biodegradable polymer and poloxamer, which are capable of regulating the rate of BST release. The coated membrane of SRIFBST was observed with a field emission scanning electron microscope. The thickness of the coated membrane was approximately $1{\mu}m$, and the pore sizes of the coated membrane surface were below $10{\mu}m$. In dissolution test, the release duration of the SRIF-BST maintained for 10 days, whereas the release duration of the control BST formula maintained for 3 days. In weight gain assay and tibia test of hypophysectomized rats, the release duration of the SRIF-BST treated group was 12 days and the net weight gain was 53.16 g, also the tibia length and strength of the SRIF-BST treated group was increased 10.5% and 23.1% compared with those of the control group, respectively.

• Biomolecules & Therapeutics
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• v.12 no.2
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• pp.57-61
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• 2004

In the present study, we investigated whether lipopolysaccharide induce mucin release and erythro-mycin affect basal and adenosine triphosphate-induced (stimulated mucin release, from airway goblet cells. Confluent primary hamster tracheal surface epithelial cells were metabolically radiolabeled and chased for 30 min or 24 hr in the presence of varying concentrations of lipopolysaccharide or erythromycin to assess the effects on $^3H$-mucin release. The results were as follows : 1) Lipopolysaccharide failed to induce mucin release, 2) Erythromycin showed no effect on both basal and stimulated mucin release during 30 min of 24 hr treatment period. We conclude that lipopolysaccharide and erythromycin can not affect mucin release by direct acting on airway mucin-secreting cells.

• Journal of Pharmaceutical Investigation
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• v.24 no.3
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• pp.139-144
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• 1994

The effect of some formulation variables on the release rate of famotidine, a $H_2$ receptor antagonist, from cellulose matrices containing hydroxypropylcellulose (HPC) in different ratios and types was investigated. The effects of tablet shape and compression pressure on dissolution rate of famotidine were studied. And the effect of the pH of dissolution media was also studied. Increase in the ratio of polymer to drug decreased the release rate of famotidine. Increase of the polymer viscosity also decreased the release rate. The release rate of famotidine was dependent on the pH of dissolution media. The release rate of drug was not much dependent on the compression pressure but dependent on the tablet shape and/or surface area. Consequently, the release rate of famotidine can be modified by changing the HPC contents, types of polymers with different viscosity grades or using appropriate fillers.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.322.1-322.1
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• 2002

Lawsone methyl ether (LME. 2-methoxy-1, 4-naphthoquinone) is a natural compound found in balsaminaceae. In this study the effect of LME on the release of renal dipeptidase (RDPase) and alkaline phosphatase (APase) known as glycosylphosphatidylinositol (GPI) anchored proteins was examined from the renal proximal tubules. Compared with control, LME (0.5mM) increased RDPase release (218%) and APase release (135%). The increase of RDPase release by LME showed concentration-dependent effect but the release pattern of APase did not. (omitted)

• The Korean Journal of Nuclear Medicine
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• v.36 no.5
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• pp.277-287
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• 2002

Purpose and Methods: We investigated the effect of ginseng total saponin (GTS) on nicotine-induced dopamine (DA) release in the striatum and nucleus accumbens of freely moving rats using in vivo microdialysis technique. Results: Systemic pretreatment with GTS decreased striatal DA release induced by local infusion of nicotine into the striatum. However, GTS had no effect on the resting levels of extracellular DA in the striatum. GTS also blocked nicotine-induced DA release in the nucleus accumbens. Conclusion: The results of the present study suggest that GTS acts on the DA terminals to prevent DA release induced by nicotine. This may reflect the blocking effect of GTS on behavioral hyperactivity induced by psychostimulants.

• The Korean Journal of Physiology
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• v.14 no.1
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• pp.25-30
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• 1980

It has been well known that beta-adrenoceptor is responsible for the renin release stimulatory and alpha-adrenoceptor may be inhibitory. It has been observed accidently that alpha-adrenergic agonist can inhibit renin release by just changing the medium temperature in Vitro experiment in this laboratory. A series of experiments were performed to clarify this interesting phenomena in Vitro experiment. Rat renal slices were incubated in PSS medium under gas phase at $37^{\circ}C$. The following results were observed. 1) Isoproterenol and norepinephrine resulted in renin release stimulatory in dose-dependent by the concentrations of $10^{-9}$ to $10^{-5}\;M/L$ at $37^{\circ}C$. 2) Norepinephrine resulted in renin release inhibitory in dose dependent by the concentrations of $10^{-7}$ to $10^{-5}\;M/L$, and almost no effect by isoproterenol $10^{-6}\;M/L$ at $20^{\circ}C$. 3) Phenoxybenzamine pretreatment at $37^{\circ}C$ accentuated isoproterenol stimulatory effect at $37^{\circ}C$. 4) Phenoxybenzamine pretreatment at $20^{\circ}C$ attenuated isoproterenol stimulatory effect at $37^{\circ}C$. These data suggest that the renal adrenoceptor(s) related to renin release maybe a single entity, and can be interconverted different forms in certain conditions.

• Textile Coloration and Finishing
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• v.9 no.2
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• pp.41-49
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• 1997

To control free formaldehyde release from fabric finished with N-methylol compounds, resin finished cotton fabric was treated with resorcinol solution, dried and cured. Factors affecting to control formaldehyde release have been investigated. It was shown that the aftertreatment with resorcinol greatly suppressed the free formaldehyde release. Up to concentration of about 5% of resorcinol, the concentration of resorcinol effected on the control of free and evolved formaldehyde. And at high concentration of resorcinol, however, the concentration became rather insensitive to contol formaldehyde release. Addition of some salt catalysts such as ammonium chloride, zinc nitrate, sodium acetate and ammonium acetate, was effective in decreasing formaldehyde release. Considering the effect on the control of formaldehyde and crease recovery, ammonium acetate was concidered to be the best catalyst. It was observed that the optimum curing temperature for the resorcinol treatment was about 15$0^{\circ}C$, and that the curing time did not affected formaldehyde release over three minutes. Although the treatment of resorcinol had a little adverse effect on crease recovery of resin finished fabric, this effect could be negligible.