• Animal cells and systems
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• v.7 no.1
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• pp.75-79
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• 2003

Highly purified high performance thin layer chromatography (HPTLC) fractions containing a putative calcium influx factor (CIF) were prepared from the Jurkat cells and Xenopus oocytes in which $Ca^{2+}$ stores were depleted by thapsigargin treatment and from the yeast in which intracellular $Ca^{2+}$ stores were also depleted by genetic means. Microinjection of the fractions has been shown to elicit $Ca^{2+}$ dependent currents in Xenopus oocytes. The nature of the membrane currents evoked by the putative CIF appeared to be carried by chloride ions since the current was blocked by the selective chloride channel blocker 1 mM niflumic acid and its reversal potential was about -24 mV. Injection of the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N, N, N',N'-tetraacetic acid (BAPTA) eradicated the current activities, suggesting the current responses are entirely $Ca^2$-dependent. Moreover, the currents were sensitive to the removal of extracellular calcium, indicating the dependence on calcium entry through the plasma membrane calcium entry channels. CIF activities were insensitive to protease, heat, and acid treatments and to Dische-reaction whereas the activities were sensitive to nucleotide pyrophosphatase and hydrazynolysis. The fraction might have a sugar because it was sensitive to Molisch test and Seliwaniff's resorcinol reaction. From the above results, CIF as a small and stable molecule seems to have pyrimidine, pyrophosphate, and a sugar moiety.oiety.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.6
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• pp.357-362
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• 2003

Carbon monoxide (CO) is low molecular weight oxide gas that is endogenously produced under physiological conditions and interacts with another gas, nitric oxide (NO), to act as a gastrointestinal messenger. The aim of this study was to determine the effects of exogenous CO on L-type calcium channel currents of human jejunal circular smooth muscle cells. Cells were voltage clamped with 10 mM barium ($Ba^{2+}$) as the charge carrier, and CO was directly applied into the bath to avoid perfusion induced effects on the recorded currents. 0.2% CO was increased barium current ($I_{Ba}$) by $15{\pm}2$% ($mean{\pm}S.E.$, p<0.01, n=11) in the cells. To determine if the effects of CO on barium current were mediated through the cGMP pathway, cells were pretreated with 1-H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, $10{mu}M$), a soluble guanylyl cyclase inhibitor, and exogenous CO (0.2%) had no effect on barium currents in the presence of ODQ ($2{\pm}1$% increase, n=6, p>0.05). CO mediates inhibitory neurotransmission through the nitric oxide pathway. Therefore, to determine if the effects of CO on L-calcium channels were also mediated through NO, cells were incubated with $N^G-nitro-L-arginine$ (L-NNA, 1 mM), a nitric oxide synthase inhibitor. After L-NNA pretreatment, 0.2 % CO did not increase barium current ($4{\pm}2$% increase, n=6, p>0.05). NO donor, SNAP ($20{\mu}M$) increased barium current by $13{\pm}2$% (n=6, p<0.05) in human jejunal smooth muscle cells. These data suggest that CO activates L-type calcium channels through NO/cGMP dependant mechanism.

• Journal of Chest Surgery
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• v.22 no.6
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• pp.901-913
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• 1989

This study was investigated under the postulation that activation of intracellular calcium- calmodulin complex during ischemia-reperfusion leads to myocardial injury. The protective effects of calcium channel blocker, diltiazem and calmodulin inhibitors, trifluoperazine, flunarizine and calmidazolium from ischemic injury in rat hearts were observed by using Langendorff apparatus when the antagonists were infused for 3 min in the beginning of ischemia. Thereby, an increase in resting tension developed during 30-min ischemia was analyzed with regard to [1] the degree of cardiac functional recovery following 60-min reperfusion, [2] changes in biochemical variables evoked during 30-min ischemia. The results obtained were as follows: l. In the ischemic group, the resting tension was increased by 4.1*0.2 g at 30-min ischemia. However, the increase in resting tension was markedly reduced not only by pretreatment with diltiazem [3.3 p M] but also with calmodulin inhibitors, trifluoperazine [3.3 p M], flunarizine [0.5 p M] and calmidazolium [0.5 p M], respectively. 2. Recovery of myocardial contractility, +dF /dt and coronary flow were much reduced when evoked by reperfusion in the ischemic group. These variables were significantly improved either by pretreatment with diltiazem or with calmodulin inhibitors. 3. The resting tension increment evoked during ischemia was significantly inversely correlated with the degree of cardiac function recovered during reperfusion. 4. Following 30-min ischemia, the production of malondialdehyde and release of lysosomal enzyme were much increased in association with a decrease in creatine kinase activity. 5. The increases in malondialdehyde production and release of free lysosomal enzyme were suppressed by pretreatment with calmodulin inhibitors as well as diltiazem. Likewise, the decrease of creatine kinase activities was prevented by these calcium antagonists. With these results, it is indicated that a increase in resting tension observed during ischemia has an inverse relationship to the cardiac function recovered following reperfusion, and further, the later may be significantly dependent on the degree of biochemical alterations occurred during ischemia such as decrease in creatine kinase activity, increased production of malondialdehyde and increased release of free lysosomal enzyme. Thus it is concluded that calmodulin plays a pivotal role in the process of ischemic injury.

• Korean Journal of Veterinary Research
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• v.34 no.1
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• pp.37-47
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• 1994

The effects of the novel compound GS-386 on the calcium current were investigated in rabbit atrial myocytes. The calcium current was recorded during various depolarizations of 200 ms duration from a holding potential of -40 mV using the whole cell patch clamp technique. The calcium current was activated from -30 mV, reached maximum amplitude at +10 mV and almost disappeared at +50 mV. Superfusion of GS-386 led to a reduction of the calcium current amplitude dose-dependently and $ED_{50}$ was $2.5{\times}10^{-7}M$. But the dependence of the calcium current on the membrane potential was not altered by GS-386. The inactivation of the calcium currents showed single exponential curves in both before and after application of GS-386. The inactivation time constants before and after application of GS-386 were almost the same(35 ms and 32.5 ms). The steady-state inactivation curve of the calcium current was not shifted by GS-386. The calcium currents both before and after application of GS-386 recovered completely in 1 sec and the recovery time constants were about 200 ms in both cases. From the above results it is concluded that the novel compound GS-386 has calcium antagonistic property decreasing the calcium current.

• Journal of Yeungnam Medical Science
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• v.32 no.1
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• pp.17-21
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• 2015

Amlodipine, a calcium channel blocker of the dihydropyridine group, is commonly used in management of hypertension, angina, and myocardial infarction. Amlodipine overdose, characterized by severe hypotension, arrythmias, and pulmonary edema, has seldom been reported in Korean literature. We report on a fatal case of amlodipine intoxication with complications including rhabdomyolysis and oliguric acute kidney injury. A 70-year-old woman with a medical history of hypertension was presented at the author's hospital 6 hours after ingestion of 50 amlodipine (norvasc) tablets (total dosage 250 mg) in an attempted suicide. Her laboratory tests showed a serum creatinine level of 2.5 mg/dL, with elevated serum creatine phosphokinase and myoglobin. The patient was initially treated with fluids, alkali, calcium gluconate, glucagon, and vasopressors without a hemodynamic effect. High-dose insulin therapy was also started with a bolus injection of regular insulin (RI), followed by continuous infusion of RI and 50% dextrose with water. Despite intensive treatment including insulin therapy, inotropics, mechanical ventilation, and continuous venovenous hemodiafiltration, the patient died of refractory shock and cardiac arrest with no signs of renal recovery 116 hours after her hospital admission.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.2
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• pp.73-77
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• 2008

Recent studies have documented that testosterone relaxes several smooth muscles by modulating $K^+$ channel activities. Smooth muscles of seminal vesicles playa fundamental role in ejaculation, which might involve testosterone. This study was aimed to assess the role of testosterone in seminal vesicular motility by studying its effects on contractile agents and on the ion channels of single vesicular myocytes in a rabbit model. The contractile responses of circular smooth muscle strips of rabbit seminal vesicles to norepinephrine ($10{\mu}M$), a high concentration of KCI (70 mM), and testosterone ($10{\mu}M$) were observed. Single vesicular myocytes of rabbit were isolated using proteolytic enzymes including collagenase and papain. Inside-out, attached, and whole-cell configurations were examined using the patch clamp technique. The applications of $10{\mu}M$ norepinephrine or 70 mM KCl induced tonic contractions, and $10{\mu}M$ testosterone (pharmacological concentration) evoked dose-dependent relaxations of these precontracted strips. Various $K^+$ channel blockers, such as tetraethylammonium (TEA; $10{\mu}M$), iberiotoxin ($0.1{\mu}M$), 4-aminopyridine (4-AP, $10{\mu}M$), or glibenclamide ($10{\mu}M$) rarely affected these relaxations. Single channel data (of inside-out and attached configurations) of BK channel activity were also hardly affected by testosterone ($10{\mu}M$). On the other hand, however, testosterone reduced L-type $Ca^{2+}$ currents significantly, and found to induce acute relaxation of seminal vesicular smooth muscle and this was mediated, at least in part, by $Ca^{2+}$ current inhibition in rabbit.

• Journal of Life Science
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• v.14 no.5
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• pp.882-890
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• 2004

Gap junction is a membrane structure facilitating the direct transmission of several ions and small molecules between two cells. It is also called an 'intercellular channel' to distinguish it from other well-known cellular channels (e.g. sodium and potassium channels). Gap junction channels are not passive conduits, rather the ion channels modulated by several stimuli including pH, calcium ion, voltage, and a chemical modification (mainly known as phosphorylation). Among them, the effects of voltage on the gating of gap junction channels have been well studied. Gap junction channels are more sensitive to the transjunctional potential ($V_j$) between two cells rather than the membrane potential($V_m$) between inside and outside the cell. In this review, I will summarize the general properties of gap junction channel and discuss the gating mechanism for the gap channels.

• Biomolecules & Therapeutics
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• v.3 no.1
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• pp.54-57
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• 1995

The effect of Ruthenium Red on the antinociceptive action of capsaicinoids was investigated using tail-flick test in mice. Capsaicin and KR-25018, when administered subcutaneously, had a potent antinociceptive effect against noxious heat stimulus. Ruthenium Red which is known to block the calcium channel coupled to the capsaicin receptor, when injected intraperitoneally more than 5 mg/kg, showed severe sedation and apparent antinociceptive effect against noxious heat stimulus. The 2.5 mg/kg Ruthenium Red, at which dose any significant sedative effect was not shown, had no effect on the antinociceptive effects of capsaicin and KR-25018. Considering this result, the antinociceptive effect of capsaicinoid may not be related to the Ruthenium Red sensitive calcium channel which is activated by capsaicin.

• Proceedings of the KIEE Conference
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• 2008.10a
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• pp.183-183
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• 2008

This paper presents the time responses of calcium ($Ca^{2+}$) ion concentration of MG-63 cells induced by a constant shear stress in micro channel were observed in the real time. Most of cells have similar rising time. There were some time delays because of the initial position of the cell in the micro channel along the pressure-driven fluid flow. The concentration of $Ca^{2+}$ exponentially decreased while time constant of each profile did not have any relation to the peak value of concentration.

• Journal of Biomedical Engineering Research
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• v.2 no.1
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• pp.3-14
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• 1981

A theoretical investigation of the origin of the spontaneous firing in the squid axon was done with a mathmatical computer modelling based on the Hodgkin-Huxley equation. It is strongly believed that the existence of calcium ions in the membrane is essential to cause firing. The results of the computer simulation of the modelling indicate that the sites of calcium ions in the membrane might be near the potassium channel and the leakage channel plays an important role in the firing. The orientation of the future research project was suggested. And also, a theoretical investigation of the origin of the firing in the propagating action potential was done in the same way.