• The Korean Journal of Physiology and Pharmacology
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• 제1권5호
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• pp.537-546
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• 1997

It has been postulated that the intracellular taurine is co-transported with $Na^+$down a concentration gradient and prevents the intracellular accumulation of sodium. It is therefore, expected that an elevated level of intracellular taurine prevents the sodium-promoted calcium influx to protect the cellular damages associated with sodium and calcium overload. In the present study, we evaluated the effects of intra- and extracellular taurine on the myocardial $Na^+$and$Ca^{++}$ contents and the cardiac functions in isolated rat hearts which were loaded with sodium by monensin, a $Na^+-ionophore$. Monensin caused a dose-dependent increase in intracellular $Na^+$ accompanied with a subsequent increase in intracellular $Ca^{++}$ and a mechanical dysfunction. In this monensin-treated heart, myocardial taurine content was decreased with a concomittent increase in the release of taurine. The monensin-induced increases in intracellular $Na^+$, $Ca^{++}$ and depression of cardiac function were prevented in the hearts of which taurine content had been increased by high-taurine diet. Conversely, in the hearts of which taurine concentration gradient had been decreased by addition of taurine in the perfusate, the monensin-induced increases in $Na^+$, $Ca^{++}$ and functional depression were accelerated. These results suggest that taurine, depending on the intra-extracellular concentration gradient, can affect intracellular sodium and calcium concentrations, and that an increased intracellular taurine may play a role in protection of myocardial dysfunction associated with the sodium and calcium overload.

• IMMUNE NETWORK
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• 제4권2호
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• pp.100-107
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• 2004

Background: The fruit of Rubus coreanus (RC), a perennial herb, has been cultivated for a long time as a popular vegetable. The anti-allergy mechanism of RC is unknown. The purpose of this study is to investigate the inhibitory effect of RC on compound 48/80- or anti-DNP IgE-induced mast cell activation. Methods: For this, influences of RC on the compound 48/80-induced degranulation, histamine release, calcium influx and the change of the intracellular cAMP (cyclic adenosine-3',5' monophosphate) levels of rat peritoneal mast cells (RPMC) and on the anti-DNP IgE-induced histamine release of RPMC were observed. Results: The pretreatment of RC inhibited compound 48/80-induced degranulation, histamine release and intracelluar calcium uptake of RPMC. The anti-DNP IgE-induced histamine release of RPMC was significantly inhibited by pretreatment of RC. The RC increased the level of intracellular cAMP of RPMC, and the pretreatment of RC inhibited compound 48/80-induced decrement of intracellular cAMP of RPMC. Conclusion: These results suggest that RC contains some substances with an activity to inhibit the compound 48/80- or anti-DNP IgE-induced mast cell activitation. The inhibitory effects of RC are likely due to the stabilization of mast cells by blocking the calcium uptake and enhancing the level of intracellular cAMP.

• Asian Pacific Journal of Cancer Prevention
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• 제17권7호
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• pp.3223-3228
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• 2016

Reports indicate that 15-deoxy-delta-12,14-prostaglandin-J2 (15d-PGJ2) has anticancer activities, but its mechanisms of action have yet to be fully elucidated. We therefore investigated the effects of 15d-PGJ2 on the human breast cancer cell lines, MCF-7 (estrogen receptor $ER{\alpha}+/ER{\beta}+$) and MDA-MB-231 ($ER{\alpha}-/ER{\beta}+$). Cellular proliferation and cytotoxicity were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays while apoptosis was determined by fluorescence microscopy and flow cytometry using annexin V-propidium iodide (PI) staining. ER expression was determined by Western blotting. Intracellular calcium was stained with Fluo-4 AM while intracellular caspase activities were detected with Caspase-$FLICA(R)$ and measured by flow cytometry. We showed that 15d-PGJ2 caused a significant increase in apoptosis in MCF-7 and MDA-MB-231 cells. $ER{\alpha}$ protein expression was reduced in treated MCF-7 cells but pre-incubation with the $ER{\alpha}$ inhibitor' ICI 182 780' did not affect the percentage of apoptotic cells. The expression of $ER{\beta}$ was unchanged in both cell lines. In addition, 15d-PGJ2 increased intracellular calcium ($Ca^{2+}$) staining and caspase 8, 9 and 3/7 activities. We therefore conclude that 15d-PGJ2 induces caspase-dependent apoptosis that is associated with an influx of intracellular $Ca^{2+}$ with no involvement of ER signaling.

• The Korean Journal of Physiology and Pharmacology
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• 제1권5호
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• pp.529-535
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• 1997

The present study was aimed at investigating whether the vascular calcium regulation is altered in hypertension. Two-kidney, one clip (2K1C) and deoxycorticosterone acetate (DOCA)-salt hypertension were made in rats, and their thoracic aortae were taken 4 weeks later. The isometric contractile response and calcium uptake of the endothelium-denuded aortic preparations were determined. Caffeine ($0.1{\sim}35\;mmol/L$) induced a greater contraction in 2K1C and DOCA-salt hypertension than in normotensive control. When the vascular calcium store was functionally-depleted by a repeated exposure to caffeine, it took longer to reload the store and to resume the initial contraction force in response to caffeine in both 2K1C and DOCA-salt hypertension. The vascular $^{45}Ca$ uptake following the functional depletion of the cellular store was also greater in both models of hypertension than in control. Ryanodine, calcium channel activator of the sarcoplasmic reticulum, attenuated the restoration of caffeine-induced vascular contraction, which was not affected by either 2K1C or DOCA-salt hypertension. Nifedipine, an L-type $Ca^{2+}$ channel blocker, attenuated the restoration of caffeine-induced contraction, which was not affected by DOCA-salt hypertension, but was more pronounced in 2K1C hypertension. Nifedipine also diminished the vascular $^{45}Ca$ uptake, which was not affected by DOCA-salt hypertension, but was more pronounced in 2K1C hypertension. Ouabain, a $Na^+,\;K^+-ATPase$ inhibitor, increased the caffeine-induced contraction by a similar magnitude in control and 2K1C hypertension, which was, however, markedly attenuated in DOCA-salt hypertension. Ouabain enhanced the vascular $^{45}Ca$ uptake, the degree of which was not affected by 2K1C hypertension, but was markedly attenuated in DOCA-salt hypertension compared with that in control. Cyclopiazonic acid, a selective inhibitor of $Ca^{2+}-ATPase$ of the sarcoplasmic reticulum, attenuated the restoration of caffeine-induced contraction, which was not affected by 2K1C hypertension, but was more marked in DOCA-salt hypertension. These results suggest that the increased vascular calcium storage may be attributed to an enhanced calcium influx in 2K1C hypertension, and to an impaired $Na^+-K^+$ pump activity of the cell membrane and subsequently increased calcium pump activity of the cellular store in DOCA-salt hypertension.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.591-598
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• 2017

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from $10-300{\mu}m$). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations ($10-100{\mu}m$) followed by secondary relaxation (at $100-300{\mu}m$). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed $CaCl_2$-induced constriction in the 60 mM $K^+$-containing $Ca^{2+}$-free solution in a dose-dependent manner. Fluorescent imaging of $Ca^{2+}$ using fluo-4 showed that a 10 min incubation with propofol ($10-300{\mu}m$) inhibited the $Ca^{2+}$ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM $K^+$-containing $Ca^{2+}$-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.

• 대한약리학회지
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• 제24권1호
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• pp.71-81
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• 1988

Glutamate와 aspartate는 단가 양이온과 칼슘에 대한 세포막의 투과성을 증가시키는 것으로 시사되고 있다. 그러나 칼슘 유입이 voltage에 의존적인 칼슘 통로에 의하여 또는 흥분성 아미노산에 활성적인 통로에 의하여 이루어지는가는 분명하지 않다. 더우기, 신경세포의 칼슘 유입에 미치는 흥분성 아미노산의 영향과 세포의 마그네슘에 대한 이들의 반응이 다른 것으로 추정하고 있다. Synaptosome에서 포타슘에 의한 칼슘 흡수는 세포외 마그네슘에 의존적이었으나 10 mM 농도에서는 그 이하의 농도에서보다 오히려 감소하였다. 소듐이 주된 반응액에서 glutamate와 aspartate에 의한 칼슘 흡수는 마그네슘에 의하여 용량에 비의존적인 양상으로 증가하였다. 그러나 NMDA의 작용은 2 mM 이상의 마그네슘에 의하여 억제되었다. 포타슘과 glutamate에 의한 칼슘 흡수는 2,4-dinitrophenol, chorpromazine과 verapami에 의하여 억제되었으나 tetraethylammonium chloride의 영향은 받지 아니하였다. Tetrodotoxin은 효과적으로 glutamate의 작용을 억제하였으나 $K^+$의 작용에는 영향을 주지 않았다. NMDA의 작용은 2,4-dinitrophenol과 tetrodotoxin에 의하여 억제되었고 verapamil에 의하여 약간 억제되었으며 tetraethylammonium chloride의 영향은 받지 아니하였다. 소듐이 주된 반응액에서 glutamate,, aspartate와 NMDA에 의한 synaptosome의 탈분극은 관찰되지 않았으나 이들은 mitochondria에서 칼슘 유입에 따른 탈분극을 초래하였다. 한편, 흥분성 아미노산은 synaptosoine의 ATPase활성도에 영향을 나타내지 않았다. 이상의 결과로부터 glutamate 또는 NMDA에 의한 synaptosome의 칼슘 흡수는 세포외 마그네슘에 각기 다른 양상을 나타내며 이들에 의한 칼슘 흡수는 포타슘을 제외한 소듐과 칼슘에 대한 세포막 투과성의 증가 그리고 이에 따른 탈분극에 연관이 있을 것으로 시사되있다.

• 한국임상수의학회지
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• 제21권3호
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• pp.291-297
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• 2004

Aminoglycosidic antibiotics have multiple effects on muscle. For example, they have been shown to block L-type $Ca^{2+}$ channels in vascular smooth muscle, cardiac muscle and skeletal muscle. Possibly as a consequence of this effect on $Ca^{2+}$ influx, they have been shown to decrease the contractility of cardiac muscle (gentamicin). The present study evaluated the effects of gentamicin on blood pressure, vasorelaxation and left ventricular pressure. Gentamicin(10, 20, 40mg/kg) produced dose-dependent blood pressure lowering in rat. The pretreatment of MgSO$_4$ and imipramine (Na$^{+}$-Mg$^{2+}$ exchange inhibitor) had no effect in gentamicin-induced hypotension. However, the gentamicin-induced hypotension was significantly potentiated in the preincubation of verapamil or nifedipine (L-type $Ca^{2+}$ channel blockers), and was significantly attenuated by CaCl$_2$ and was slightly attenuated by caffeine (phosphodiesterase inhibitor). Gentamicin (10, 30, 100$\mu$g/m1) did not have an effect on relaxation of phenylephrine-precontracted aortic rings but high concentration of gentamicin(100, 300$\mu$g/ml) relaxed KCl-precontracted aortic rings, which relaxation was potentiated by treatment of nifedipine. Whereas gentamicin markedly decreased left ventricular developed pressure (LVDP) in perfused heart. These data suggest that gentamicin has significant blood pressure lowering of the rat, which seems to be mediated by calcium channel-sensitive pathway and blood $Ca^{2+}$ level may be important role in this response.

• Journal of Photoscience
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• 제6권2호
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• pp.77-83
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• 1999

Calcium has a variety of functions in neuron and muscle cells and blood clotting, especially in the visual system where dark adapted rods cotransport with Na$\^$+/ into the cell. An influx of Ca$\^$++/ flows out of the cell through the Na$\^$+/-Ca$\^$++/ exchanger. By using a modified Using chamber in order to bring in vivo environment close, we have known that Ca$\^$++/ blocks the activity of guanylate cyclase, in consequence, having an effect on the amplitude of electroretinogram (ERG). We have measured the Ca$\^$++/, K$\^$+/, and Na$\^$+/ concentration in dark and light adapted bullfrog＇s (Rana catesbeiana) vitreous humor. The calcium concentration of the light adapted bullfrog＇s vitreous humor was higher than that of the dark adapted bullfrog＇s vitreous humor This means that ion activity between the photoreceptor and vitreous humor side is light dependent and we have found that a Ca$\^$++/ channel and Ca$\^$++/K$\^$+/ exchanger exist in the vitreous humor side. Taken together permeability of Ca$\^$++/, K$\^$+/ and K$\^$+/ ion internal limiting membrane faced in the vitreous humor side has light-dependent activity during the illumination.

• Preventive Nutrition and Food Science
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• 제21권4호
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• pp.323-329
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• 2016

Achyranthes japonica Nakai (AJN) water extract has a variety of physiological properties, including anti-diabetic, anti-cancer, anti-inflammatory, anti-microbial, and anti-oxidative activities. In the present study, the inhibitory effects of AJN extract were investigated in high affinity immunoglobulin E receptor ($Fc{\varepsilon}RI$)-mediated KU812F cells activation. AJN extract showed suppressive effects on histamine release and intracellular calcium [$Ca^{2+}$]i elevation from anti$Fc{\varepsilon}RI$ antibody (CRA-1)-stimulated cells in a dose-dependent manner. Flow cytometric analysis showed that AJN extract treatment caused a dose-dependent decrease in the cell surface $Fc{\varepsilon}RI$ expression and the binding between the cell surface $Fc{\varepsilon}RI$ and the IgE antibody. Moreover, reverse transcription-polymerase chain reaction analysis showed that levels of the mRNA for the $Fc{\varepsilon}RI$ ${\alpha}$ chain was decreased by treatment with AJN extract. These results indicate that AJN extract may exert anti-allergic effects via the inhibition of calcium influx and histamine release, which occurs as a result from the downregulation of the binding of IgE antibody to cell surface $Fc{\varepsilon}RI$. This mechanism may occur through $Fc{\varepsilon}RI$ expression inhibition.

• Journal of Microbiology
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• 제34권3호
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• pp.253-269
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• 1996

Infection of fish cells with IHNV resulted in gradual increase in cytosolic free Ca$\^$2+/ concentration ([Ca$\^$2+/)] in CHSE, gradual decrease in [Ca$\^$2+/] in FHM, and no significant change in RTG cells. The degree of [Ca$\^$2+/] increase or decrease was dependent on the amount of infectious virus, and these [Ca$\^$2+/] variations were maximal at 16 hours after virus infection (p. i.) in both cell lines. When the fish cells were infected with inactivated IHNV, evident variation in [Ca$\^$2+/] was not observed. Thus, infectivity of IHNV appears to correlate with changes in [Ca$\^$2+/] in virus-infected cells. These IHNV-induced [Ca$\^$2+/] changes were partially blocked by cycloheximide, but not affected by cordycepin. It seems to be that virus-induced Ca$\^$2+/ variations were more related with protein synthesis than RNA synthesis. Various Ca$\^$2+/ related drugs were used in search for the mechanisms of the [Ca$\^$2+/], changes following IHNV infection of CHSE cells. Decreasing extracellular Ca$\^$2+/ concentration or blocking Ca$\^$2+/ influx from extracellular media inhibited the IHNV-induced increase in [Ca$\^$2+/], in CHSE cells. Similar results were obtained with intracellular Ca$\^$2+/ sources are important in IHNV-induced [Ca$\^$2+/] increase in CHSE cells.