• Animal cells and systems
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• 제3권2호
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• pp.103-113
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• 1999

Many in-depth reviews related to regulations of prolactin secretion are available. We will, therefore, focus on controversial aspects using personal opinion in this review. The neuroendocrine control of prolactin secretion from the anterior pituitary gland involves multiple factors including prolactin-release inhibiting factor (PIF) and prolactin releasing factor (PRF). The PIF exerts a tonic inhibitory control in the physiological conditions. The PIF should be able to effectively inhibit prolactin release or a lifetime, but the inhibitory action of dopamine cannot be sustained for a long period of time. Perifusion of a high concentration of dopamine (l ,000 nM) could not sustain inhibitory action on prolactin release but when a small amount of ascorbic acid (0.1 mM) is added in a low concentration of dopamine (3 nM) solution, prolactin release was inhibited for a long period. Ascorbate is essential for dopamine action to inhibit prolactin release. We have, therefore, concluded that the PIF is dopamine plus ascorbate. The major transduction system for dopamine to inhibit prolactin release is the adenylyl cyclase system. Dopamine decreases cyclic AMP concentration by inhibiting adenylyl cyclase, and cyclic AMP stimulates prolactin release. However, the inhibitory mechanism of dopamine on prolactin release is much more complex than simple inhibition of CAMP production. The dopamine not only inhibits cyclic AMP synthesis but also inhibits prolactin release by acting on a link(s) after the CAMP event in a chain reaction for inhibiting prolactin release. Low concentrations of dopamine stimulate prolactin release. Lactotropes are made of several different subtypes of cells and several different dopamine receptors are found in pituitary. The inhibitory and stimulatory actions induced by dopamine can be generated by different subtype of receptors. The GH$_4$ZR$_7$ cells express only the short isoform (D$_{2s}$) of the dopamine receptor, as a result of transfecting the D$_{2s}$ receptors into GH$_4$C$_1$ cells which do not express any dopamine receptors. When dopamine stimulates or inhibits prolactin release in GH$_4$ZR$_7$ cells, it is clear that the dopamine should act on dopamine D$_{2s}$ receptors since there is no other dopamine receptor in the GH$_4$ZR$_7$. Dopamine is able to stimulate prolactin release in a relatively low concentration while it inhibits in a high concentration in GH$_4$ZR$_7$. These observations indicate that the dopamine D$_2$ receptor can activate stimulatory and/or inhibitory transduction system depending upon dopamine concentrations.

• Animal cells and systems
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• 제7권4호
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• pp.309-315
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• 2003

Renal dipeptidase (RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19) has been widely studied since it was first purified from porcine kidney brush border membrane. It was reported that RDPase activity in urine samples of acute and chronic renal failure patients decreases. Nitric oxide (NO) is a highly reactive free radical involved in a number of physiological and pathological processes. NO is able to act in a dual mode, leading either to induction of apoptosis or to blunted execution of programmed cell death. NO inhibited the RDPase release from porcine renal proximal tubules, which could be blocked by L-NAME. Chitosan, the linear polymer of D-glucosamine in $\beta$(1\longrightarrow4) linkage, not only reversed the decreased RDPase release by NO but also increased NO production in the proximal tubule cells. The stimulatory effect of NO on RDPase release from proximal tubules in the presence of chitosan must be different from the previously proposed mechanism of RDPase release via NO signaling pathway. Chitosan stimulated the RDPase release in the proximal tubules and increased RDPase activity to 220% and 250% at 0.1% and 1%, respectively. RDPase release was decreased to about 40% in the injured proximal tubules and was recovered in proportion to the increase of chitosan. Chitosan may be useful in recovery of renal function from $HgCl_2$injury.

• 대한치과교정학회지
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• 제24권1호
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• pp.115-123
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• 1994

To study bone resorption mechanism, effect of LPS on the $^{45}Ca$ release from fetal rat ulnae and radii, and effects of carbonic anhydrase inhibitors on the LPS-induced bone resorption in organ culture were studied. Ulnae and radii were removed from 19 day old fetal rats, prelabelled by subcutaneous injection of $200{\mu}Ci\;^{45}CaCl_2$ into their mother on the 17th day of gestation. Radioactivities of $^{45}Ca$ released into media were determined after 24, 48 and 72 hours. Effects of LPS and carbonic anhydrase inhibitors were observed by the ratio of $\%$ release of $^{45}Ca$ between paired control and experimental group. The observed results were as follows : 1. $LPS(1{\mu}g/ml)$ supplemented in media for 72hours increased the $^{45}Ca$ release significantly after 48 and 72 hours of culture and $LPS(10{\mu}g/m1)$ increased the $^{45}Ca$ release significantly after 72 hours of culture. 2. LPS-induced $^{45}Ca$ release was not inhibited significantly by 1mM sulfanilamide but inhibited significantly by 10mM sulfanilamide after 48 and 72 hours of culture. 3. LPS-induced $^{45}Ca$ release was not inhibited significantly by 0.1mM dichlorphenamide but inhibited significantly by 1mM dichlorphenamide after 48 and 72 hours of culture. 4. LPS-induced $^{45}Ca$ release was not inhibited significantly by 1mM acetazolamide but inhibited sighificantly by 5mM acetazolamide after 72 hours of culture.

• The Korean Journal of Physiology and Pharmacology
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• 제13권1호
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• pp.23-26
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• 2009

During operations, neurosurgeons usually perform multiple temporary occlusions of parental artery, possibly resulting in the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this study, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion(VO) model to compare between single occlusion and repeated transient occlusions within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. From real time monitoring of glutamate release in 11 VO model, the change of extracellular glutamate level in repeated transient occlusion group was smaller than that of single occlusion group, and the onset time of glutamate release in the second ischemic episode of repeated occlusion group was delayed compared to the first ischemic episode which was similar to that of single 10 min ischemic episode. These results suggested that repeated transient occlusion induces less glutamate release from neuronal cell than single occlusion, and the delayed onset time of glutamate release is attributed to endogeneous protective mechanism of ischemic tolerance.

• Archives of Pharmacal Research
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• 제29권6호
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• pp.508-513
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• 2006

The effect of acteoside, a phenylpropanoid glycoside isolated from Clerodendron trichotomum Thunberg, on histamine and arachidonic acid release was investigated in RBL 2H3 cells. Histamine was dose-dependently released from RBL 2H3 cells by melittin, arachidonic acid and thapsigargin. In extracellular $Ca^{2+}-free$ solution, basal secretion of histamins increased by two fold. The response of histamine release to melittin and thapsigargin in $Ca^{2+}-free$ solution was significantly decreased, whereas the response to arachidonic acid was significantly increased as compared with those in normal solution. Acteoside inhibited histamine release induced by melittin, arachidonic acid and thapsigargin in a dose-dependent manner in the presence or absence of extracellular $Ca^{2+}$. However, the inhibitory activity of acteoside was more potent in normal solution than that in $Ca^{2+}-free$ solution. These data suggest that inhibitory mechanism of acteoside on histamine release may be related to extracellular $Ca^{2+}$. On the other hand, acteoside significantly inhibited arachidonic acid release and prostaglandin $E_2$ production Induced by $0.5\;{\mu}M$ melittin. It is possible that acteoside may be developed as an anti-inflammatory agent.

• Archives of Pharmacal Research
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• 제21권6호
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• pp.664-670
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• 1998

The role of intracellular $Ca^{2+}$, in the regulation of tumor cell proliferation by products of arachidonic acid (AA) metabolism was investigated using U-373 MG human as trocytoma cells. Treatment with nordihydroguaiaretic acid (NDGA), a lipoxygenase (LOX) inhibitor, or caffeic acid (CA), a specific 5-LOX inhibitor, suppressed proliferation of the tumor cells in a dose-dependent manner. However, indomethacin (indo), a cyclooxygenase (COX) inhibitor, did not significantly alter proliferation of the tumor cells. At anti-proliferative concentrations, NDGA and CA significantly inhibited intracellular $Ca^{2+}$ release induced by carbachol, a known intracelluar $Ca^{2+}$ agonist in the tumor cells. Exogenous administration of leukotriene $B_4(LTB_4)$, an AA metabolite of LOX pathway, enhanced proliferation of the tumor cells in a concentration-dependent fashion. In addition, $LTB_4$, induced intracelluar $Ca^{2+}$ release. Intracellular $Ca^{2+}$-inhibitors, such as an intracellular $Ca^{2+}$ chelator (BAPTA) and intracellular $Ca^{2+}$-release inhibitors (dantrolene and TMB-8), significantly blocked the LTB4-induced enhancement of cell proliferation and intracellular $Ca^{2+}$ release. These results suggest that LOX activity may be critical for cell proliferation of the human astrocytoma cells and that intracelluar $Ca^{2+}$ may play a major role in the mechanism of action of LOX.

• Archives of Pharmacal Research
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• 제25권6호
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• pp.932-939
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• 2002

The aim of the present study was to determine the characteristics of cytisine on the secretion of catecholamines (CA) in isolated perfused rat adrenal glands, and to clarify its mechanism of action. The release of CA evoked by the continuous infusion of cytisine ($1.5{\times}10^{-5} M$) was time-dependently reduced from 15 min following the initiation of cytisine infusion. Furthermore, upon the repeated injection of cytisine ($5{\times}10^{-5}$), at 30 min intervals into an adrenal vein, the secretion of CA was rapidly decreased following the second injection. Tachyphylaxis to the release of CA was observed by the repeated administration of cytisine. The cytisine-induced secretion of CA was markedly inhibited by pretreatment with chlorisondamine, nicardipine, TMB-8, and the perfusion of $Ca^{2+}$-free Krebs solution, while it was not affected by pirenzepine or diphenhydramine. Moreover, the secretion of CA evoked by ACh was time-dependently inhibited by the prior perfusion of cytisine ($5{\times}10^{-6} M$). Taken together, these experimental data suggest that cytisine causes secretion of catecholamines from the perfused rat adrenal glands in a calcium-dependent fashion through the activation of neuronal nicotinic ACh receptors located in adrenomedullary chromaffin cells. It also seems that the cytisine-evoked release of catecholamine is not relevant to the activation of cholinergic M$_1$-muscarinic or histaminergic receptors.

• Macromolecular Research
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• 제17권12호
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• pp.1010-1014
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• 2009

Monodispersed microparticles with a poly(D,L-lactide-co-glycolide) (PLGA) core and a poly(ethyl 2-cyanoacrylate) (PE2CA) shell were prepared by Shirasu porous glass (SPG) membrane emulsification to reduce the initial burst release of doxorubicin (DOX). Solution mixtures with different weight ratios of PLGA polymer and E2CA monomer were permeated under pressure through an SPG membrane with $1.9\;{\mu}m$ pore size into a continuous water phase with sodium lauryl sulfate as a surfactant. Core-shell structured microparticles were formed by the mechanism of anionic interfacial polymerization of E2CA and precipitation of both polymers. The average diameter of the resulting microparticles with various PLGA:E2CA ratios ranged from 1.42 to $2.73\;{\mu}m$. The morphology and core-shell structure of the microparticles were observed by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The DOX release profiles revealed that the microparticles with an equivalent PLGA:E2CA weight ratio of 1:1 exhibited the optimal condition to reduce the initial burst of DOX. The initial release rate of DOX was dependent on the PLGA:E2CA ratio, and was minimized at a 1:1 ratio.

• 한국군사과학기술학회지
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• 제11권3호
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• pp.161-168
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• 2008

The deployable space structure is necessary to minimize the satellite volume and launch cost. For the deployment, passive deployment mechanism has widely been used to attenuate a latch shock induced when the structure is just fully deployed. To reduce the latch shock, viscous damper is applied to the passive deployment mechanism and it can control the deployment speed of the structure. In this paper, dynamic analysis of the deployable space structure using the passive deployment mechanism with the viscous damper has been performed. The viscous damping values have been optimized through numerical simulation. The satellite's attitude influenced by pyro activation for the release of the structure has also been investigated.

• Biomolecules & Therapeutics
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• 제16권2호
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• pp.147-160
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• 2008

The present study was designed to examine effects of polyphenolic compounds isolated from red wine (PCRW) on the release of catecholamines (CA) from the isolated perfused model of the rat adrenal medulla, and to clarify its mechanism of action. PCRW (20${\sim}$180 ${\mu}$g/mL), given into an adrenal vein for 90 min, caused inhibition of the CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic $N_N$ receptor agonist, 100 ${\mu}$M) and McN-A-343 (a selective muscarinic $M_1$ receptor agonist, 100 ${\mu}$M) in dose- and time-dependent fashion. PCRW itself did not affect basal CA secretion (data not shown). Following the perfusion of PCRW (60 ${\mu}$g/mL), the secretory responses of CA evoked by Bay-K-8644 (a L-type dihydropyridine $Ca^{2+}$ channel activator, 10 ${\mu}$M), cyclopiazonic acid (a cytoplasmic $Ca^{2+}$-ATPase inhibitor, 10 ${\mu}$M) and veratridine (an activator of voltage-dependent $Na^+$ channels, 10 ${\mu}$M) were also markedly blocked, respectively. Interestingly, in the simultaneous presence of PCRW (60 ${\mu}$g/mL) and L-NAME (a selective inhibitor of NO synthase, 30 ${\mu}$M), the inhibitory responses of PCRW on the CA secretion evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclpiazonic acid were recovered to considerable level of the corresponding control release compared with those effects of PCRW-treatment alone. Practically, the amount of NO released from adrenal medulla after loading of PCRW (180 ${\mu}$g/mL) was significantly increased in comparison to the corresponding basal released level. Collectively, these results obtained here demonstrate that PCRW inhibits the CA secretory responses evoked by stimulation of cholinergic (both muscarinic and nicotinic) receptors as well as by direct membrane-depolarization from the isolated perfused adrenal gland of the normotensive rats. It seems that this inhibitory effect of PCRW is mediated by blocking the influx of both ions through $Na^+$ and $Ca^+{2$} channels into the rat adrenomedullary chromaffin cells as well as by inhibiting the release of $Ca^{2+}$ from the cytoplasmic calcium store, which are due at least partly to the increased NO production through the activation of nitric oxide synthase. Based on these data, it is also thought that PCRW may be beneficial to prevent or alleviate the cardiovascular diseases, such as hypertension and angina pectoris.