• Title/Summary/Keyword: $Ca^{2+ }$ / peak current

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Effects of Bay K, cAMP and Isoprenaline on the Na-Ca Exchange Current of Single Rabbit Atrial Cells (토끼 심방근에서 Na-Ca 교환 전류에 대한 Bay K, cAMP, Isoprenaline 효과)

  • Ho, Won-Kyung;Earm, Yung-E
    • The Korean Journal of Physiology
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    • v.24 no.2
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    • pp.377-388
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    • 1990
  • Ca movements during the late plateau phase in rabbit atrium implicate Na-Ca exchange. In single atrial cells isolated from the rabbit the properties of the inward current of Na-Ca exchange were investigated using the whole cell voltage clamp technique. The inward currents were recorded during repolarization following brief 2 ms depolarizing pulse to +40 mV from a holding potential of -70 mV. Followings are the results obtained: 1) When stimulated every 30 sec, the inward currents were activated and reached peak values $6{\sim}12\;ms$ after the beginning of depolarizing pulse. The mean current amplitude was 342 pA/cell. 2) The current decayed spontaneously from the peak activation and the timecourse of the relaxation showed two different phases: fast and slow phase. 3) The recovery of the inward current was tested by paired pulse of various interval. The peak current recovered exponentialy with a time course similar to that of Ca current recovery. 4) Relaxation timecourse was also affected by pulse interval and time constant was reduced almost linearly according to the decrease of pulse interval between 30 sec and 1 sec. 5) The peak inward current was increased by long prepulse stimulation, Bay K, isoprenaline or c-AMP. 6) The relaxation time constant of the inward current was prolonged by Bay K or c-AMP, and shortened by isoprenaline. From the above results, it could be concluded that increase of the calcium current potentiates and prolongs intracellular calcium transients, while shortening of the timecourse by isoprenaline or short interval stimulations might be due to the facilitation of Ca uptake by SR.

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Inactivation of N-Type Calcium Current in Rat Sympathetic Neurons

  • Goo, Yong-Sook;Keith S. Elmslie
    • Proceedings of the Korean Biophysical Society Conference
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    • 1999.06a
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    • pp.52-52
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    • 1999
  • Inactivation of N-type calcium current has been reported to be voltage dependent (Jones & Marks, 1989) and $Ca^{2+}$ dependent(Cox & Dunlap, 1994). We examined inactivation by recording currents from the same cell both in [B $a^{2+}$]$_{o}$ and [C $a^{2+}$]$_{o}$ in rat sympathetic neurons. With 11 mM internal EGTA, fractional inactivation[l-(current amplitude at the end of 5 sec pulse/peak current amplitude [1-(current amplitude at the end of 5 sec pulse/peak current amplitude)] was larger in $Ca^{2+}$(0.80$\pm$0.07) than in $Ba^{2+}$(0.69$\pm$0.10)(n=31, p<0.001), but the current traces were nicely fitted with two exponential components both in $Ba^{2+}$ and $Ca^{2+}$.(omitted)ted)ted)

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The Properties of Na-Ca Exchange Current in Single Atrial Cells of ,The Rabbit (토끼 단일 심방근 세포에서 Na-Ca 교환전류의 특성에 관한 연구)

  • Youm, Wook;Ho, Won-Kyung;Suh, Kyung-Phill
    • Journal of Chest Surgery
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    • v.22 no.4
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    • pp.548-561
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    • 1989
  • In single atrial cells isolated from the rabbit the properties of inward current of Na-Ca exchange were investigated using the whole cell voltage clamp technique. The current was recorded during repolarization following brief 2 ms depolarizing pulse to +40 mV from a holding potential of * 70 mV. Followings are the results obtained: 1. When stimulated every 30 seconds, the inward currents were activated and reached peak values 6-12 ms after the beginning of depolarizing pulse. The mean current amplitude was 342 pA/cell. 2. The current decayed spontaneously from the peak activation and the time course of the relaxation showed two different phases fast and slow phase. The time constants were 10-18 ms and 60-140 ms, respectively. 3. The recovery of inward current was tested by paired pulse of various intervals. The peak current recovered exponentially with time constant of 140 ms and 1 p M isoprenaline accelerated the recovery process. 4. Relaxation time course was also affected by pulse interval and time constant of the fast phase was reduced almost linearly according to the decrease of pulse interval between 30 sec and 1 sec. 5. The peak activation was increased in magnitude by long prepulse stimulation, 5 p M Bay K, 1 p M isoprenaline or internal and external application of c-AMP. 6. The relaxation time constant of the fast phase was prolonged by 5 p M Bay K or c-AMP, and shortened by isoprenaline. However the time course of the slow relaxation phase was not so much changed. From the above results, it could be concluded that increase of the calcium current by Bay K or c-AMP results in the potentiation and prolongation of intracellular calcium transient, and the facilitation of Ca uptake by SR might be a mechanism of shortening the time constant of current relaxation by short interval stimulation or isoprenaline.

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Effect of Fluid Pressure on L-type $Ca^{2+}$ Current in Rat Ventricular Myocytes (백서 심실 근세포 L형 $Ca^{2+}$ 전류에 대한 유체압력의 효과)

  • Lee Sun-Woo;Woo Sun-Hee
    • YAKHAK HOEJI
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    • v.50 no.2
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    • pp.111-117
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    • 2006
  • Cardiac chambers serve as mechanosensory systems during the haemodynamic or mechanical disturbances. To examine a possible role of fluid pressure (FP) in the regulatien of atrial $Ca^{2+}$ signaling we investigated the effect of FP on L-type $Ca^{2+}$ current $(I_{Ca})$ in rat ventricular myocytes using whole-cell patch-clamp technique. FP $(\sim40cm\;H_2O)$ was applied to whole area of single myocytes with electronically controlled micro-jet system. FP suppressed the magnitude of peak $I_{Ca}$ by $\cong25\%$ at 0 mV without changing voltage dependence of the current-voltage relationship. FP significantly accelerated slow component in inactivation of $I_{Ca}$, but not its fast component. Analysis of steady-state inactivation curve revealed a reduction of the number of $Ca^{2+}$ channels available for activity in the presence of FP. Dialysis of myocytes with high concentration of immobile $Ca^{2+}$ buffer partially attenuated the FP-induced suppression of $I_{Ca}$. In addition, the intracellular $Ca^{2+}$ buttering abolished the FP-induced acceleration of slow component in $I_{Ca}$ inactivation. These results indicate that FP sup-presses $Ca^{2+}$ currents, in part, by increasing cytosolic $Ca^{2+}$ concentration.

A study on the behavior of charge particles of $(SR.Ca)TiO_3$ ceramic ($(SR.Ca)TiO_3$세라믹의 하전입자 거동에 관한 연구)

  • 김진사;최운식;신철기;김성열;박현빈;김태성;이준응
    • Electrical & Electronic Materials
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    • v.10 no.2
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    • pp.97-104
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    • 1997
  • In this paper, in order to investigate the behavior of charged particles on (Sr.Ca)TiO$_{3}$ ceramics with paraelectric properties, the characteristics of electrical conduction and thermally stimulated current was measured respectively. As a result, the conduction mechanism is divided into three regions having different mechanism as the current increased. The region I below 200[V/Cm] shows the ohmic conduction. The region B between 200[V/cm] and 2000[V/cm] can be explained by the Poole-Frenkel emission theory, and the region III above 2000[V/cm] is dominated by the tunneling effect. The three peaks of TSC were obtained at the temperature of -20[.deg. C], 20[.deg. C] and 80[.deg. C], respectively. The origins of these peaks are that the .alpha. peak observed at -20[.deg. C] looks like to be ascribed to the ionization excitation from donor level in the grain, and the .alpha.' peak observed at 20 [.deg. C] appears to show up by hopping conduction of the trapped carrier of border between the oxidation layer and the grain, and the .betha. peak observed at 80[.deg. C] seems to be resulted from hopping conduction of existing carrier in the trap site of the border between the oxidation and second phase.

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Forward-Mode $Na^+-Ca^{2+}$ Exchange during Depolarization in the Rat Ventricular Myocytes with High EGTA

  • Kim, Eun-Gi;Ko, Chang-Mann
    • The Korean Journal of Physiology and Pharmacology
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    • v.5 no.6
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    • pp.487-494
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    • 2001
  • During depolarization, extrusion of $Ca^{2+}$ from sarcoplasmic reticulum through forward-mode $Na^+-Ca^{2+}$ exchange was studied in the rat ventricular myocytes patch-clamped in whole-cell configuration. In order to confine the $Ca^{2+}$ responses in a micro-domain by limiting the $Ca^{2+}$ diffusion time, rat ventricular myocytes were dialyzed with high (14 mM) EGTA. $K^+$ current was suppressed by substituting KCl with 105 mM CsCl and 20 mM TEA in the pipette filling solution and by omitting KCl in the external Tyrode solution. $Cl^-$ current was suppressed by adding 0.1 mM DIDS in the external Tyrode solution. During stimulation roughly mimicking action potential, the initial outward current was converted into inward current, $47{\pm}1%$ of which was suppressed by 0.1 mM $CdCl_2.$ 10 mM caffeine increased the remaining inward current after $CdCl_2$ in a cAMP-dependent manner. This caffeine-induced inward current was blocked by $1\;{\mu}M$ ryanodine, $10\;{\mu}M$ thapsigargin, 5 mM $NiCl_2,$ or by $Na^+\;and\;Ca^{2+}$ omission, but not by $0.1\;{\mu}M$ isoproterenol. The $I{\sim}V$ relationship of the caffeine-induced current elicited inward current from -45 mV to +3 mV with the peak at -25 mV. Taken together, it is concluded that, during activation of the rat ventricular myocyte, forward-mode $Na^+-Ca^{2+}$ exchange extrudes a fraction of $Ca^{2+}$ released from sarcoplasmic reticulum mainly by voltage-sensitive release mechanism in a micro-domain in the t-tubule, which is functionally separable from global $Ca^{2+}{_i}$ by EGTA.

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Heterogeneity of the SR-dependent Inward $Na^+-Ca^{2+}$ Exchange Current in the Heavily $Ca^{2+}-buffered$ Rat Ventricular Myocytes

  • Yoon, Kyung-Bong;Ahn, Sung-Wan;Ko, Chang-Mann
    • The Korean Journal of Physiology and Pharmacology
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    • v.8 no.2
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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 $Ca^{2+}-induced-Ca^{2+}\;release$.

Effect of Dietary Calcium Levels on Peak Bone Mass Formation in Growing Female Rats (칼슘 섭취 수준이 성장기 암컷 흰쥐의 최대골질량 형성에 미치는 영향)

  • 이연숙;박미나;김은미
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.26 no.3
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    • pp.480-487
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    • 1997
  • The present study was designed to examine how Ca intake contributes to the increase of peak bone mass with growing female rats. Weaned rats were fed experimental diets consisting in five levels of Ca; very low(0.1%), low(0.2%), moderate(0.5%), high(1.0%) and very high(1.5%) for 4, 8 and 12 weeks. Bone growth, metabolism and Ca metabolism were determined. As for the rats fed for 4 weeks, the bone weight, length and breaking force and bone metabolism were not significantly affected by dietary Ca levels, whereas the current intakes of Ca were observed to have significantly affected the rats fed for 8 or 12 weeks with regard to the bone weight, length and breaking force and bone metabolism. The bone ash and Ca contents of the rats were affected by dietary Ca levels for the total period of feeding. It is suggested that dietary Ca itself affected the mineralization process either during the growth or later, although the resulting bone mass is not a linear function of dietary Ca content.

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A Study on the Behavior of Charged Particles of $(1-x)(SrPb)(CaMg)TiO_3-Bi_2O_3{\cdot}3TiO_2$ Ceramics ($(1-x)(SrPb)(CaMg)TiO_3-xBi_2O_3{\cdot}3TiO_2$ 세라믹의 하전입자 거동에 관한 연구)

  • Kim, Chung-Hyeok;Choi, Woon-Shik;Jung, Il-Hyung;Chung, Kue-Hye;Lee, Joon-Ung
    • Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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    • 1992.11a
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    • pp.34-37
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    • 1992
  • In this paper, the $(SrPb)(CaMg)TiO_3$-xBi_2O_3{\cdot}3TiO_2$ ceramics with paraelectric properties were fabricated by the mixed oxide method. In order to investigate the behavior of charged particles, the characteristics of electrical conduction and thermally stimulated current were measured respectively. As a result on characteristics of the electrical conduction, the leakage current was increased as measuring temperature was increased. At room temperature, the conduction current was divided into the three steps as a function of DC electric field. The first step was Ohmic region due to ionic conduction, below 15[kV/cm]. The second step was showed a saturation which seems to be related to a depolarizing field occuring in field-enforced ferroelectric phase, between 15[kV/cm] and 40[kV/cm]. The third step was attributed to Child's law related to spare charge which injected from electrode, above 40[kV/cm]. Thermally stimulated currents(TSC) spectra with various biasing fields exhibited three distinguished peaks that were denoted as ${\alpha}$, ${\alpha}'$ and ${\beta}$ peak, each of which appeared at nearby -30, 20 and 95[$^{\circ}C$] respectively. It is confirmed that the a peak was due to trap electron trapped in the grainboundary, and ${\alpha}'$ peak that was observed above only 1.5[kV/mm] was attributed to field-enforced ferroelectric polarization. The origin of ${\beta}$ peak was identified as ion migration which caused the degradation.

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17 beta-Estradiol Increases Peak of $\textrm{Ca}^{2+}$ Current in Mouse Early Embryo (에스트로겐이 생쥐 초기배의 $\textrm{Ca}^{2+}$ 전류에 미치는 영향)

  • 강다원;신용원;김은심;홍성근;한재희
    • Journal of Embryo Transfer
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    • v.16 no.2
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    • pp.79-89
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    • 2001
  • Steroid hormones control the expression of many cellular regulators, and a role thor estrogen in mouse oocytes has been well documented. The preovulatory $E_2$increment is generally accepted as the endocrine process regulating induction of in vivo oocyte maturation To address whether the activity of the T-type $Ca^{2+}$ channel is altered by 17 beta-estradiol ( $E_2$), we examined the actions of $E_2$on the calcium channel of mouse oocytes and early embryos. Oocrtes were collected from the oviduct of mice treated with pregnant mare's serum gonadotropin (PMSG) and human choronic gonadotropin (hCG). Whole cell voltage clamp technique and confocal microscopy were used to examine that $E_2$increase intracellular $Ca^{2+}$ concentration ([C $a^{2+}$]$_{i}$ ) via voltage dependent $Ca^{2+}$ channel (VDC) and estrogen receptor (FSR), and $E_2$concentration by the use of radioimmunoassay (RIA) were examined in mouse. The results obtained were as follows: The peak of $Ca^{2+}$ current induced by $E_2$increased 122% to 1.50$\pm$0.03 nA from 1.23$\pm$0.21 nA (n=15) in the presence of 5 mM extracellular $Ca^{2+}$ concentration ([C $a^{2+}$]$_{o}$ ). The increased $Ca^{2+}$ current was temporally associated with $Ca^{2+}$ transients. The intracellular $Ca^{2+}$ level increased 207%~30 s following the addition of 1${\mu}{\textrm}{m}$ $E_2$(relative fluorescence intensity: 836.4$\pm$131.2 for control, n=10, 1736.4$\pm$192.0 in the presence of $E_2$, n=10). $E_2$increased amplitude of $Ca^{2+}$ current and [C $a^{2+}$]$_{i}$ . $E_2$-induced $Ca^{2+}$ current and $E_2$concentration in blood were showed difference on the stage of embryo. These results suggest that $E_2$modulate $Ca^{2+}$ channel to increase $Ca^{2+}$ influx.$Ca^{2+}$ influx.

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