• The Korean Journal of Physiology and Pharmacology
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• 제9권2호
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• pp.95-101
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• 2005

In the heart, $Na^{+}-Ca^{2+}$ exchange (NCX) is the major $Ca^{2+}$ extrusion mechanism. NCX has been considered as a relaxation mechanism, as it reduces global $[Ca^{2+}]_i$ raised during activation. However, if NCX locates in the close proximity to the ryanodine receptor, then NCX would curtail $Ca^{2+}$ before its diffusion to global $Ca^{2+}_i$ This will result in a global $[Ca^{2+}]_i$ decrease especially during its ascending phase rather than descending phase. Therefore, NCX would decrease the myocardial contractility rather than inducing relaxation in the heart. This possibility was examined in this study by comparing NCX-induced extrusion of $Ca^{2+}$ after its release from SR in the presence and absence of global $Ca^{2+}_i$ transient in the isolated single rat ventricular myocytes by using patch-clamp technique in a whole-cell configuration. Global $Ca^{2+}_i$ transient was controlled by an internal dialysis with different concentrations of BAPTA added in the pipette. During stimulation with a ramp pulse from +100 mV to -100 mV for 200 ms, global $Ca^{2+}_i$ transient was suppressed only mildly, and completely at 1 mmol/L, and 10 mmol/L BAPTA, respectively. In these situations, ryanodine-sensitive inward NCX current was compared using $100{\mu}mol/L$ ryanodine, $Na^+$ depletion, 5 mmol/L $NaCl_2$ and $1{\mu}mol/L$ nifedipine. Surprisingly, the result showed that the ryanodine-sensitive inward NCX current was well preserved after 10 mmol/L BAPTA to 91 % of that obtained after 1 mmol/L BAPTA. From this result, it is concluded that most of the NCX-induced $Ca^{2+}$ extrusion occurs before the $Ca^{2+}$ diffuses to global $Ca^{2+})i$ in the rat ventricular myocyte.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 1999년도 학술발표회 진행표 및 논문초록
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• pp.65-65
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• 1999

Na$^{＋}$-Ca$^{2＋}$ Exchanger is known to playa critical role in the regulation of intracellular $Ca^{2＋}$ in many tissues and cells. In heart, the Na$^{＋}$-Ca$^{2＋}$ exchange is the principal $Ca^{2＋}$ extrusion mechanism and affects cardiac excitation-contraction coupling. To understand the functional role of cardiac Na$^{＋}$ -Ca$^{2＋}$ exchanger (NCXl) in vivo, we tried to ablate the cardiac Na$^{2+}$-Ca$^{2+}$ exchanger gene locus by the use of the gene targeting technologies.(omitted)ted)

• The Korean Journal of Physiology and Pharmacology
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• 제8권2호
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• pp.101-110
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• 2004

Voltage-sensitive release mechanism was pharmacologically dissected from the $Ca^{2+}-induced\;Ca^{2+}\;release$ in the SR $Ca^{2+}$ release in the rat ventricular myocytes patch-clamped in a whole-cell mode. SR $Ca^{2+}$ release process was monitored by using forward-mode $Na^+-Ca^{2+}$ exchange after restriction of the interactions between $Ca^{2+}$ from SR and $Na^+-Ca^{2+}$ exchange within micro-domains with heavy cytosolic $Ca^{2+}$ buffering with 10 mM BAPTA. During stimulation every 10 s with a pulse roughly mimicking action potential, the initial outward current gradually turned into a huge inward current of $-12.9{\pm}0.5\;pA/pF$. From the inward current, two different inward $I_{NCX}s$ were identified. One was $10\;{\mu}M$ ryanodine-sensitive, constituting $14.2{\pm}2.3%$. It was completely blocked by $CdCl_2$ (0.1 mM and 0.5 mM) and by $Na^+-depletion$. The other was identified by 5 mM $NiCl_2$ after suppression of $I_{CaL}$ and ryanodine receptor, constituting $14.8{\pm}1.6%$. This latter was blocked by either 10 mM caffeine-induced SR $Ca^{2+}-depletion$ or 1 mM tetracaine. IV-relationships illustrated that the latter was activated until the peak in $30{\sim}35\;mV$ lower voltages than the former. Overall, it was concluded that the SR $Ca^{2+}$ release process in the rat ventricular myocytes is mediated by the voltage-sensitive release mechanism in addition to the $Ca^{2+}-induced-Ca^{2+}\;release$.

• 한국토양비료학회지
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• 제23권2호
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• pp.107-113
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• 1990

주요(主要) 석회물질(石灰物質)이 해성염토(海成鹽土)의 제염(除鹽)에 주는 효과(效果)를 밝히기 위(爲)하여 염토(鹽土)가 함유(含有)하는 Na + Mg와 당량(當量)의 Ca를 탄산(炭酸)칼슘, 수산화(水酸化)칼슘, 규산(珪酸)칼슘 또는 석고(石膏)로 시용(施用)하여 유리원통시험(圓筒試驗)을 실시(實施)하였다. 최상층(最上層) 1/10염토(鹽土)에 석회물질(石灰物質) 반량(半量)을 혼합(混合)하고 남은 반량(半量)을 표면(表面)에 덮은 후 (後) 증류수(蒸溜水)를 주가(注加)하면서 연속적(連續的)으로 3차에 걸쳐 여과수(濾過水)를 받아 세척(洗滌)한 층별토양(層別土壤)과 함께 분석(分析)하였는 바 그 결과(結果)는 아래와 같다. 1. $CaSO_4$는 투수(透水)와 제염(除鹽)(Na)을 용역(容易)하게 하였으나 Mg를 하층(下層)에 집적(集積)시켰다. 2. $Ca(OH)_2$, $CaCO_3$, $CaCO_3$는 표층(表層)에 Mg를 침전(沈澱)시키고, 하위층(下位層)에서 Mg를 세탈(洗脫)하였는데, 특(特)히 표층직하(表層直下)에서 더 세탈(洗脫)하였다. 이 세탈(洗脫)은 $Ca(OH)_2$처리(處理)에서 가장 현저(顯著)했고, $CaSiO_2$, $CaCO_3$의 순서(順序)로 약(弱)해졌다. 3. 치환성(置換性) Na의 해리(解離)에 더한 석회(石灰)의 알칼리성(性)은 토양(土壤)의 pH를 높였으며, 투수속도(透水速度)를 낮추고 Na의 제염(除鹽)을 저해(沮害)하였다. 이 영향(影響)은 $Ca(OH)_2$처리(處理)에서 더 컸다. 4. 세탈(洗脫)된 토양(土壤)의 pH는 치환성(置換性) Na 및 Mg와 다음 회부관계(回復關係)를 보였다. $$pH=7.77+0.489Na/\sqrt{Mg}\;r=0.845^{**}$$.

• The Korean Journal of Physiology and Pharmacology
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• 제11권5호
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• pp.183-188
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• 2007

Using BHK cells with stable expression of cardiac $Na^+/Ca^{2+}$ exchanger(BHK-NCX1), reverse mode(i.e. $Ca^{2+}$ influx mode) of NCX1 current was recorded by whole-cell patch clamp. Repeated stimulation of reverse NCX1 produced a cytosolic $Ca^{2+}$-dependent long-term inactivation of the exchanger activity. The degrees of inactivation correlated with NCX1 densities of the cells and were attenuated by reduced $Ca^{2+}$ influx via the reverse exchanger. The inactivation of NCX1 was attenuated by(i) inhibition of $Ca^{2+}$ influx with reduced extracellular $Ca^{2+}$, (ii) treatment with NCX1 blocker($Na^{2+}$), and (iii) increase of cytoplasmic $Ca^{2+}$ buffer(EGTA). In BHK-NCX1 cells transiently expressing TRPV1 channels, $Ca^{2+}$ influx elicited by capsaicin produced a marked inactivation of NCX1. We suggest that cytoplasmic $Ca^{2+}$ has a dual effect on NCX1 activities, and that allosteric $Ca^{2+}$ activation of NCX1 can be opposed by the $Ca^{2+}$-dependent long-term inactivation in intact cells.

• The Korean Journal of Physiology and Pharmacology
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• 제2권6호
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• pp.715-724
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• 1998

Frequency-force relationships (FFR) were studied in electrically field stimulated rat left atria (LA) by reducing the stimulation frequency from resting 3 Hz to test frequencies (0.1-1 Hz) for 5 minutes. The twitch amplitudes of LA elicited the typical negative staircases with 3-phased changes: the initial rapid increase, the second decrease and the following plateau at test frequencies. Verapamil $(3{\times}10^{-5}\;M)$ pretreatment elicited frequency-dependent suppression of the twitch amplitudes, exaggerating the negative staircase. Monensin pretreatment enhanced not the peak but the plateau amplitudes in a concentration-dependent manner. When the $Na^+-Ca^{2+}$ exchange was blocked by $Na^+\;and\;Ca^{2+}$ depletion in the Krebs Hensleit buffer (0 $Na^+-0\;Ca^{2+}$ KHB), the twitch amplitudes increased in a frequency-dependent manner, changing the negtive staircase into the positve one. Meanwhile, the 0 $Na^+-0\;Ca^{2+}$ KHB applicationinduced enhancement was strongly suppressed by caffeine (5 mM) pretreatment. Only dibucaine among the local anesthetics increased the basal tone during frequency reduciton. There were no differences in $^{45}Ca$ uptakes between 0.3 Hz and 3 Hz stimulation except at 1 min when it was significantly low at 0.3 Hz than 3 Hz, illustrating net $Ca^{2+}$ losses. Monensin pretreatment enhanced the rate of this $Ca^{2+}$ loss. Taken together, it is concluded that $Na^+-Ca^{2+}$ exchange extrudes more SR released $Ca^{2+}$ out of the cell in proportion to the frequency, resulting in the negative rate staircase in the rat LA.

• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2000년도 춘계학술발표대회
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• pp.203-206
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• 2000

Bifidobacteria의 배양효율을 증대하기 위하여 완충제로써 $CaCO_3$를 Ca-alginate에 고정화한 비드를 제조하여 사용하였다. B. longum KCTC 3218과 한국인 분변에서 분리한 B. longum HLC 3742 균주를 $CaCO_3$ 비드, NaOH, $Na_2CO_3$, $NH_4OH$ 등을 완충제로 각각 사용한 2.5-liter 발효기에서 각각 배양하여 균 증식과 저장에 따른 생존력을 조사한 결과 $CaCO_3$ 비드를 완충제로 사용한 경우가 다른 완충제를 사용한 경우보다 균 증식과 저장 안정성에서 효과적임을 알 수 있었다. 따라서 완충제로써 $CaCO_3$ 비드는 bifidobacteria의 고농도 배양과 생존력 증대에 유용할 것으로 사료되었다.

• The Korean Journal of Physiology and Pharmacology
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• 제14권1호
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• pp.51-57
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• 2010

It was hypothesized that NaF induces calcium sensitization in $Ca^{2+}$-controlled solution in permeabilized rat mesenteric arteries. Rat mesenteric arteries were permeabilized with $\beta$-escin and subjected to tension measurement. NaF potentiated the concentration-response curves to $Ca^{2+}$ (decreased $EC_{50}$ and increased $E_{max}$). Cumulative addition of NaF (4.0, 8.0 and 16 mM) also increased vascular tension in $Ca^{2+}$-controlled solution at pCa 7.0 or pCa 6.5, but not at pCa 8.0. NaF-induced vasocontraction and $GTP{\gamma}S$-induced vasocontraction were not additive. NaF-induced vasocontraction at pCa 7.0 was inhibited by pretreatment with Rho kinase inhibitors H1152 or Y27632 but not with a MLCK inhibitor ML-7 or a PKC inhibitor Ro31-8220. NaF induces calcium sensitization in a $Ca^{2+}$ dependent manner in $\beta$-escin-permeabilized rat mesenteric arteries. These results suggest that NaF is an activator of the Rho kinase signaling pathway during vascular contraction.

• 한국세라믹학회지
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• 제36권10호
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• pp.1087-1093
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• 1999

Bioglass which is one of the surface active bionmaterials has a good biocompatibility but a poor mechanical strength, In the present work therefore two types of fluoride-containing bioglasses were coated on an alumina to improve mechanical strength. Crystallization of the coating layer and the hydroxyapatite formation on the bioactive glass coatings in tris-buffer solution were studied. When bioactive glass coated alumina was heat-treated Na2CaSi3O8 crystal was formed on the layer at lower temperature while wollastonite(CaSIO3) was obtained at higher temperature. Hydroxyapatite forming rate on the coating layer with Na2CaSi3O8 crystal was delayed with SiO2 contents in glass composition. However the hydroxyapatite was developed in 20minutes regardless SiO2 contents when the coating layer crystallized into wollastonite. More amount of P3+ ions were leached out of the coating layer with wollastonite than that with Na2CaSi3O8 crystal while Na+ and Ca2+ ions were leached out more easily from the Na2CaSi3O8 crystal containing coating layer.

• The Korean Journal of Physiology
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• 제20권1호
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• pp.125-133
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• 1986

Ethanol이 고양이 회장 종주근의 수축에 미치는 영향을 관찰한 결과 정상 Tyrode용액에서는 $0.5{\pm}4%$ 범위내에서 자발적 수축 및 기초장력을 억제하였으나 $Na^+$이 surcose로 대치된 용액에서는 수축을 유발시켰다. 이러한 수축은 ethanol의 농도에 비례하여 증가하였으며 용액내의 Na-free 용액으로 처리한 기간이 길수록 증가하였다. 용액내 $Ca^{2+}$이 없는 경우에도 ethanol에 의한 수축은 $La{+3}$에 의해 억제되었으나 verapamil을 전처치한 후 Na-free액을 처리했을 때는 수축이 나타나지를 않았다. Ethanol은 $^45Ca$의 유출에는 어떤 영향을 나타내지는 못하였다. 이상의 결과로 보아 Na-free용액에서 ethanol은 세포막에 결합하고 있는 $Ca^{2+}$이나 세포내부에 결합하고 있는 $Ca^{2+}$의 세포내로 유리를 증가시켜 수축을 유발시키는 것으로 사료된다.