• Title/Summary/Keyword: Na-K pump

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$Na^{+}$-dependent NADH:quinone Oxidoreductase in the Respiratory Chain of the Marine Bacterium Marinomonas vaga

  • Kim, Young-Jae;Park, Yong-Ha
    • Journal of Microbiology and Biotechnology
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    • v.6 no.6
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    • pp.391-396
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    • 1996
  • The Gram-negative marine bacterium Marinomonas vaga, which requires 0.5 M NaCl concentration for optimal growth, is slightly halophilic. The growth of M vaga was highly resistant to the proton conductor, carbonyl cyanide m-chlorophenylhydrazone (CCCP) under alkaline pH conditions (pH 8.5) but very sensitive to CCCP under acidic pH conditions (pH 6.5). These results suggest that the respiratory chain-linked NADH oxidase system of M. vaga may lead to generation of a $Na^{+}$ electrochemical gradient. In order to examine the existence of $Na^{+}$-stimulated NADH oxidase in M. vaga, membrane fractions were prepared by the osmotic lysis method. The membrane-bound NADH oxidase oxidized both NADH and deamino-NADH as substrates and required $Na^{+}$ for maximum activity. The maximum activity of NADH oxidase was obtained at about pH 8.5 in the presence of 0.2 M NaCl. The site of $Na^{+}$-dependent activation in the NADH oxidase system was at the NADH:quinone oxidoreductase segment. The NADH oxidase and NADH:quinone oxidoreductase were very sensitive to the respiratory chain inhibitor, 2-heptyl-4-hydroxyquinoline-N-oxide (HQNO) in the presence of 0.2 M NaCl but highly resistant to another respiratory inhibitor, rotenone. Based on these findings, we conclude that M. vaga possesses the $Na^{+}$-dependent NADH:quinone oxidoreductase that may function as an electrogenic $Na^{+}$ pump.

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The Action of Acetylcholine on the End-Plate Potential

  • Koh, Il-Sup
    • The Korean Journal of Physiology
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    • v.9 no.2
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    • pp.41-48
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    • 1975
  • The failure of the action potential at the end-plate membrane to reach the sodium equilibrium potential is due to the stimulating action of acetylcholine on $Na^+-K^+$ pump. This action of acetylcholine causes an enormous increase in the $K^+$ transport rate. The quantitative amount of potassium ions in the inside of the end-plate membrane prevented the permeability of sodium ions during the depolarization phase of the action potential. It would favor the changes in the shape of action potential by acetylcholine which are always toward a fixed potential slightly below the zero line. The increased $Na^+-K^+$ pump activity by acetylcholine is responsible for the hypopolarization of membrane. This reduces the membrane resistance of the end-plate during transmitter activity.

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Active Transport Characteristics of K+-Na+ Pumping System in Cell Membrane Model which Irradiated by High Energy X-ray (고에너지 엑스선을 조사한 세포막모델에서 K+-Na+ 펌프 시스템의 능동적 전달 특성)

  • Ko, In-Ho
    • Journal of the Korean Society of Radiology
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    • v.11 no.2
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    • pp.157-165
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    • 2017
  • The active transport characteristics of $K^+$ and $Na^+$ pumping system of cell membrane model which irradiated by high energy x-ray(linac 6MeV) was investigated. The cell membrane model used in this experiment was a $Na^+$ type sulfonated copolymerized membrane of styrene and divinylbenezene. The initial flux of the ion was increased with increase of both $H^+$ ion concentration. In this experiment range(pH 1.5-5, temperature $36.5^{\circ}C$), the initial flux of $K^+$ which was not irradiated by radiation was found to be from $2.09{\times}10^{-4}$ to $1.32{\times}10^{-3}mole/cm^2{\cdot}h$ and that of $Na^+$ from $7.09{\times}10^{-4}$ to $1.09{\times}10^{-3}mole/cm^2{\cdot}h$. the initial flux of $K^+$ which was irradiated by radiation was found to be from $21.0{\times}10^{-4}$ to $16.7{\times}10^{-3}mole/cm^2{\cdot}h$ and that of $Na^+$ from $62.0{\times}10^{-4}$ to $20.6{\times}10^{-3}mole/cm^2{\cdot}h$. The ratio $K^+$/$Na^+$ of membrane was about 1.10. And the driving force of pH of irradiated membrane was significantly increased about 9-20 times than membrane which was not irradiated. As active transport of $K^+$ and $Na^+$ of cell membrane model were abnormal, cell damages were appeared at cell.

The altered $Na^+,\;K^+$-pump activity following the fumonisin exposure to LLC-PKl cells

  • Choi, Heon-Kyo;Yoo, Jae-Myung;Tudev, Munkhtsetseg;Lee, Yong-Moon;Yun, Yeo-Pyo;Yoo, Hwan-Soo
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.110.1-110.1
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    • 2003
  • Fumonisins are specific inhibitors of ceramide synthase in sphingolipid metabolism. Sphingolipids are biologically active lipid mediators in cellular physiology and involved in cell signaling, growth, transformation, angiogenesis and differentiation. The objective of this study was to determine the effect of fumonisin B1 on $Na^+, \;K^+$-pump activity when fumonisin B1 was exposed to LLC-PK1 cells. Fumonisin B1 elevated free sphingoid bases and their 1-phosphates, while total complex sphingolipids were depleted at 20$\mu$M fumonisin B1 during the 3 day exposure. (omitted)

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Possible Implication for an Indirect Interaction between Basic Fibroblast Growth Factor and (Na,K)ATPase

  • Oh, Ji-Hyun;Lee, Kyung-Lim
    • Archives of Pharmacal Research
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    • v.21 no.6
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    • pp.707-711
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    • 1998
  • The (Na,K)ATPase is responsible for generating the ionic gradients and membrane potentials by the exchange of intracellular $Na^+$ for $K^+$. It has been recentl y shown that (Na,K)ATPase is involved in the exocytic pathway of basic fibroblast growth factor (bFGF), although it is not known that bFGF is secreted to the outside of cell through direct interaction with (Na,K) ATPase. To understand the role for (Na,K)ATPase in the secretary pathway of bFGF, we have sought to identify the cytoplasmic domains of the alpha1 isoform of (Na,K)ATPase interacting with bFGF by yeast two-hybrid system. We have also investigated the interaction between the alpha2 isoform of (Na,K)ATPase and bFGF to find out whether the interaction is isoform-specific. We found that none of the cytoplasmic domains of (Na,K)ATPase isoforms interacted with bFGF. The result suggests that the interaction between bFGF and (Na,K)ATPase might be indirect, thus requiring other proteins which are involved in the formation of protein complexes for the interaction, although we cannot exclude the possibility that the interaction requires the element of the whole alpha subunit structure that was not present in the isolated alpha subunit cytoplasmic domains.

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Effects of ${\alpha}_1-Adrenergic$ Stimulation on Contractility and Intracellular $Na^+$ Activity of Guinea Pig Ventricular Muscles (기니픽 심근의 수축력과 세포내 $Na^+$ 활성도에 미치는 ${\alpha}_1-Adrenergic$ 수용체 자극효과)

  • Kim, Jin-Sang;Kang, Hyung-Sub;Chae, Soo-Wan;Lee, Chin-Ok
    • The Korean Journal of Pharmacology
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    • v.32 no.2
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    • pp.189-199
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    • 1996
  • Myocardial ${\alpha}_1-adrenoceptors$ have been shown to mediate a biphaslc inotropic response that was characterized by a transient decline followed by a sustained increasing phase in guinea pig ventricular muscle. Recently one group reported that an ${\alpha}_1-adrenoceptors-induced$ intracellular $Na^+$ decrease is linked to fast $Na^+$ channel inhibition and another group reported that it is linked to $Na^+$-$K^+$ pump activation by ${\alpha}_{1b}-adrenoceptors$. But until now, its mechanism is not clear. Therefore, to see whether the $Na^+$channel or $Na^+-K^+$ pump is related to a decrease in intracellular $Na^+$ activity and/or the negative inotropic response, and which ${\alpha}_1-adrenoceptor$ subtype was involved in the decrease in intracellular $Na^+$activity by phenylephrine, we used conventional and sodium selective microelectrodes, and tension transducer to determine the effects of ${\alpha}_1-adrenergic$ stimulation on membrane potential, intracellular $Na^+$ activity, and twitch force in guinea pig ventricular muscles. $10^{-5}$ M Phenylephrine produced a slight hyperpolarization of the diastolic membrane potential, a decrease or increase in $a_N^i_a$, and a biphasic inotropic response. The negative inotropic response accompanied by a decrease in intracellular $Na^+$activity, whereas in muscles showing a remarkable positive inotropic response without initial negative inotropic effect was accompanied by an increase in intracellular $Na^+$ activity. The decrease in intracellular $Na^+$ activity was apparently inhibited by WB4101, an antagonist of the ${\alpha}_{1a}-adrenoceptors$. The decrease in intracellular $Na^+$ activity caused by phenylephrine was not abolished or reduced by a block of the fast $Na^+$ channels. $V_{max}$ also was not affected by phenylephrine. Phenylephrine produced an increase in intracellular $Na^+$ activity in the presence of a high concentration of extracellular $Ca^{2+}$ (in quiescent muscle) or phorbol dibutyrate, a protein kinase C activator(in beating muscle). These suggest that the ${\alpha}_{1a}-adrenoceptors-mediated$ decrease in intracellular $Na^+$ activity may be related to the protein kinase C.

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Effect of sodium on transmembrane calcium movement in the cat ileal longitudinal muscle

  • Rho, Young-Jae;Yun, Il;Kang, Jung-Sook
    • Archives of Pharmacal Research
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    • v.10 no.2
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    • pp.80-87
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    • 1987
  • To get a better insight into the exxistence and the role of a Na-Ca exchange mechanism in smooth muscle, the effect of Na substitution with sucrose on tension development, cellular Ca uptake and $^{45}Ca$ efflux was investigated using isolated cat ileal longitudinal muscle strips. Experimental results were summarized as follows;1) Exposure of the cat ileal longitudinal muscle to Na-free solution induced a contraction, and the magnitude of the contraction increased after incubation of the muscle strips with ouabain ($2{\times10^{-}5}$M) for 1hr. 2) Cellular Ca uptake in Na-free solution increased with an increase in Na content of the Na-loading media, and a linear relationship existed between tissue Na content and cellular Ca uptake for 10 min 3) After tissues were equilibrated in PSS containing $^{45}Ca$ for 2hr, cellular Ca uptake decreased with rising the external Na concentration. 4)Removal of medium Na or inhibition of the Na-K pump decreased the rate of $^{45}Ca$ efflux. These results strongly suggested that Na substitution increases cellular Ca uptake and decreases the rate of $^{45}Ca$ efflux via a Na-Ca exchange mechanism.

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Fabrication of Charge-pump Active-matrix OLED Display Panel with 64 ${\times}$ 64 Pixels

  • Na, Se-Hwan;Shim, Jae-Hoon;Kwak, Mi-Young;Seo, Jong-Wook
    • Journal of Information Display
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    • v.7 no.1
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    • pp.35-40
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    • 2006
  • Organic light-emitting diode (OLED) display panel using the charge-pump (CP) pixel addressing scheme was fabricated, and the results show that it is applicable for information display. A CP-OLED panel with 64 ${\times}$ 64 pixels consisting of thin-film capacitors and amorphous silicon Schottky diodes was fabricated using conventional thin-film processes. The pixel drive circuit passes electrical current into the OLED cell during most of the frame period as in the thin-film transistor (TFT)-based active-matrix (AM) OLED displays. In this study, the panel was operated at a voltage level of below 4 V, and this operation voltage can be reduced by eliminating the overlap capacitance between the column bus line and the common electrode.

Update on Medical Treatment of GERD/LPR (위식도역류질환과 인후두역류질환의 약물 요법에 대한 최신지견)

  • Kim, Mi-Na;Kim, Joo-Sung
    • Korean Journal of Bronchoesophagology
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    • v.16 no.2
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    • pp.97-104
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    • 2010
  • Gastroesophageal reflux disease (GERD) is a common disorder caused by the reflux of gastric contents into the esophagus. According to the recent classification, GERD can elicit esophageal and extraesophageal syndromes. Laryngopharyngeal reflux (LPR) is defined as laryngeal symptoms with laryngeal inflammation caused by the acid reflux. The prevalence of GERD and LPR is increasing during the past decades in Korea and management of GERD and LPR is a challenging issue in clinical practice. Proton pump inhibitor is the most effective drug in the treatment of GERD. Most patients with LPR are given a 2-month trial of a proton pump inhibitor (PPI), however, there is still little evidence on the diagnosis or the treatment of LPR. During the last years concern have been raised regarding the risk of averse events related to long-term use of PPI. We review the recent update on medical treatment of GERD/LPR.

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Altered Cardiac $Na^+,K^+$-ATPase Activity in Prehypertensive Spontaneously Hypertensive Rat

  • Lee, Shin-Woong;Lee, Jeung-Soo;Wallick, Earl-T.
    • Archives of Pharmacal Research
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    • v.16 no.4
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    • pp.305-311
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    • 1993
  • $Na^+,K^+$-ATPase activity, $Na^+$-dependent phosphorylation, and $[^3H]$ ouabain binding in sarcolemma prepared from 4 week old spontaneously hypertensive rat(SHR) ventricles were compared to the same parameters in sarcolemma from age matched nomotensive Wister-Kyoto (WKY) rat ventricles to examine whether the reduced myocardial $Na^+$-pump activity in SHR is an inherited enzymatic defect or a second phenomenon due to sustained hypertension. The total body weights, ventricular weights, and blood pressures were the same for SHR and WKY. No significant differences in sarcolemmal protein content and protein recovery were noted between the two groups. Sarcolemma isolated from SHR ventricles showed significantly less $Na^+,K^+$-ATPase activity ande number of phosphorylation sites when compared to sarcolemma from the WKY ventricles. Equilibrium binding of $[^3H]$ouabain and the tumover number of myocardial $Na^+,K^+$-ATPase, however, were the same for both groups. These reults indicate that the low affinity $(\alpha,\;or\;\alpha^1)\;\alpha$ isoform is the same in ventricles of SHR and WKY. The reduced amount of isoform of the $Na^+,K^+$-ATPase inprehypetensive SHR ventricles may play some role in the development of hypertension.

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