• Title/Summary/Keyword: [Ca$^{}$ 2+/]$_{i}$

Search Result 1,766, Processing Time 0.037 seconds

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
    • /
    • v.8 no.2
    • /
    • pp.101-110
    • /
    • 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 $Ca^{2+}-induced-Ca^{2+}\;release$.

Two Types of Voltage-activated Calcium Currents in Goldfish Horizontal Cells

  • Paik, Sun-Sook;Bai, Sun-Ho;Jung, Chang-Sub
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.9 no.5
    • /
    • pp.269-273
    • /
    • 2005
  • In horizontal cells (HCs) that were freshly dissociated from goldfish retina, two types of voltagedependent calcium currents ($I_{Ca}$) were recorded using a patch-clamping configuration: a transient type current and a sustained type current. The cell was held at -40 mV, and the prepulse step of -90 mV was applied before command pulse between -65 and +55 mV. The transient $Ca^{2+}$ current was activated by depolarization to around -50 mV from a prepulse voltage of -90 mV lasting at least 400 ms and reached a maximal value near -25 mV. On the other hand, the sustained $Ca^{2+}$ current was induced by pre-inactivation for less than 10 ms duration. Its activation started near -10 mV and peaked at +20 mV. $Co^{2+}$ (2 mM) suppressed both of these two components, but nifedipine ($20{\mu}M$), L-type $Ca^{2+}$ channel antagonist, blocked only the sustained current. Based on the activation voltage and the pharmacolog$I_{Ca}$l specificity, the sustained current appears to be similar to L-type $I_{Ca}$ and the transient type to T-type $I_{Ca}$. This study is the first to confirm that transient type $I_{Ca}$ together with the sustained one is present in HCs dissociated from goldfish retina.

Pharmacological Evidence that Cromakalim Inhibits $Ca^{2+}$ Release from Intracellular Stores in Porcine Coronary Artery

  • Rhim, Byung-Yong;Hong, Sun-Hwa;Kim, Chi-Dae;Lee, Won-Suk;Hong, Ki-Whan
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.1 no.1
    • /
    • pp.27-34
    • /
    • 1997
  • In the present study, it was aimed to further indentify the intracellular action mechansm of cromakalim and levcromakalim in the porcine coronary artery. In intact porcine coronary arterial strips loaded with fura-2/AM, acetylcholine caused an increase in intracellular free $Ca^{2+}$ $([Ca^{2+}]_i)$ in association with a contraction in a concentration-dependent manner. Cromakalim (1 ${\mu}M$) caused a reduction in acetylcholine-induced increased $[Ca^{2+}]_i$ not only in the mormal physiological salt solution (PSS) but also in $Ca^{2+}$-free PSS (containing 1 mM EGTA). In the skinned strips prepared by exposure of tissue to 20 .${\mu}M$ B-escin, inositol 1,4,5-trisphosphate ($IP_3$) evoked an increase in $[Ca^{2+}]_i$, but it was without effect on the intact strips. The $IP_3$-induced increase in $[Ca^{2+}]_i$ was inhibited by cromakalim by 78% and levcromakalim by 59% (1 .${\mu}M$, each). Pretreatment with glibenclamide (a blocker of ATP-sensitive $K^+$ channels, 10 .${\mu}M$) and apamin (a blocker of small conductance $Ca^{2+}$-activated $K^+$ channels, 1 .${\mu}M$) strongly blocked the effect of cromakalim and levcromakalim. However, charybdotoxin (a blocker of large conductance $Ca^{2+}$-activated $K^+$ channels, 1 .${\mu}M$) was without effect. In addition, cromakalim inhibited the $GTP{\gamma}S$ (100 .${\mu}M$, non-hydrolysable analogue of GTP)-induced increase in $[Ca^{2+}]_i$. Based on these results, it is suggested that cromakalim and levcromakalim exert a potent vasorelaxation, in part, by acting on the $K^+$ channels of the intracellular sites (e.g., sarcoplasmic reticulum membrane), thereby, resulting in decrease in release of $Ca^{2+}$ from the intracellular storage site.

  • PDF

Dual Effect of $H_2O_2$ on the Regulation of Cholecystokinin-induced Amylase Release in Rat Pancreatic Acinar Cells

  • An, Jeong-Mi;Rhie, Jin-Hak;Seo, Jeong-Taeg
    • International Journal of Oral Biology
    • /
    • v.31 no.4
    • /
    • pp.127-133
    • /
    • 2006
  • [ $H_2O_2$ ], a member of reactive oxygen species (ROS), is known to be involved in the mediation of physiological functions in a variety of cell types. However, little has been known about the physiological role of $H_2O_2$ in exocrine cells. Therefore, in the present study, the effect of $H_2O_2$ on cholecystokinin (CCK)-evoked $Ca^{2+}$ mobilization and amylase release was investigated in rat pancreatic acinar cells. Stimulation of the acinar cells with sulfated octapeptide form of CCK (CCK-8S) induced biphasic increase in amylase release. Addition of $30\;{\mu}M\;H_2O_2$ enhanced amylase release caused by 10 pM CCK-8S, but inhibited the amylase release induced by CCK-8S at concentrations higher than 100 pM. An ROS scavenger, $10\;{\mu}M$ Mn(III)tetrakis(4-benzoic acid)porphyrin chloride, increased amylase release caused by CCK-8S at concentrations higher than 100 pM, although lower concentrations of CCK-8S-induced amylase release was not affected. To examine whether the effect of $H_2O_2$ on CCK-8S-induced amylase release was exerted via modulation of intracellular $Ca^{2+}$ signaling, we measured the changes in intracellular $Ca^{2+}$ concentration $([Ca^{2+}]_i)$ in fura-2 loaded acinar cells. Although $30\;{\mu}M\;H_2O_2$ did not induce any increase in $[Ca^{2+}]_i$ by itself, it increased the frequency and amplitude of $[Ca^{2+}]_i$ oscillations caused by 10 pM CCK-8S. However, $30\;{\mu}M\;H_2O_2$ had little effect on 1 nM CCK-8S-induced increase in $[Ca^{2+}]_i$. ROS scavenger, 1 mM N-acetylcysteine, did not affect $[Ca^{2+}]_i$ changes induced by 10 pM or 1 nM CCK-8S. Therefore, it was concluded that $30\;{\mu}M\;H_2O_2$ enhanced low concentration of CCK-8S-induced amylase release probably by increasing $[Ca^{2+}]_i$ oscillations while it inhibited high concentration of CCK-8S-induced amylase release.

Catalytic Effects on Graphitized Carbon Fibers of Graphitization Catalysts Introduced during Hot-Water Stretching (열수 연신시 흑연화 촉매 도입에 따른 탄소섬유의 흑연화 촉진효과)

  • Hyun-Jae Cho;Hye Rin Lee;Byoung-Suhk, Kim;Yong-Sik, Chung
    • Composites Research
    • /
    • v.37 no.3
    • /
    • pp.162-169
    • /
    • 2024
  • In this study, PAN(polyacrylonitrile)-based precursor fibers were produced through a wet-spinning process, and their morphologies and graphitization behavior were investigated in the presence of two graphitization catalysts (Ca, Ni). The graphitization catalysts were introduced into the formed pores during hot-water stretching of wet-spun PAN-based precursor fibers. The catalytic effects of graphitization catalysts were examined through crystal structure and Raman analysis. At a relatively low temperature of 1500℃, the graphitization was not significantly affected, whereas at a high temperature of 2400℃, the obtained ID/IG value of graphite fiber (GF-Ni100) was decreased by about twice (~0.28) compared to the untreated fibers (GF-AS~0.54). By comparing the ID/IG values (GF-Ca100~0.42: GF-Ni100~0.28) of Ca and Ni graphitization catalyst, it was found that the degree of graphitization of Ni graphitization catalyst showed higher influence than that of Ca graphitization catalyst. Moreover, 2D band was also observed, indicating that the graphite plane structures composed of multiple layers were developed. XRD results confirmed that the crystal inter-planar distance (d002) of the graphite crystal was slightly decreased after the treatment with the graphitization catalyst, But, the crystal size of Ca-treated graphite fiber (GF-Ca100) was increased by up to ~5 nm.

Comparison of electrophysiological effects of calcium channel blockers on cardiac repolarization

  • Lee, Hyang-Ae;Hyun, Sung-Ae;Park, Sung-Gurl;Kim, Ki-Suk;Kim, Sung Joon
    • The Korean Journal of Physiology and Pharmacology
    • /
    • v.20 no.1
    • /
    • pp.119-127
    • /
    • 2016
  • Dihydropyridine (DHP) calcium channel blockers (CCBs) have been widely used to treat of several cardiovascular diseases. An excessive shortening of action potential duration (APD) due to the reduction of $Ca^{2+}$ channel current ($I_{Ca}$) might increase the risk of arrhythmia. In this study we investigated the electrophysiological effects of nicardipine (NIC), isradipine (ISR), and amlodipine (AML) on the cardiac APD in rabbit Purkinje fibers, voltage-gated $K^+$ channel currents ($I_{Kr}$, $I_{Ks}$) and voltage-gated $Na^+$ channel current ($I_{Na}$). The concentration-dependent inhibition of $Ca^{2+}$ channel currents ($I_{Ca}$) was examined in rat cardiomyocytes; these CCBs have similar potency on $I_{Ca}$ channel blocking with $IC_{50}$ (the half-maximum inhibiting concentration) values of 0.142, 0.229, and 0.227 nM on NIC, ISR, and AML, respectively. However, ISR shortened both $APD_{50}$ and $APD_{90}$ already at $1{\mu}M$ whereas NIC and AML shortened $APD_{50}$ but not $APD_{90}$ up to $30{\mu}M$. According to ion channel studies, NIC and AML concentration-dependently inhibited $I_{Kr}$ and $I_{Ks}$ while ISR had only partial inhibitory effects (<50% at $30{\mu}M$). Inhibition of $I_{Na}$ was similarly observed in the three CCBs. Since the $I_{Kr}$ and $I_{Ks}$ mainly contribute to cardiac repolarization, their inhibition by NIC and AML could compensate for the AP shortening effects due to the block of $I_{Ca}$.

Protective Effect of Fangchinoline on Cyanide-Induced Neuro-toxicity in Cultured Rat Cerebellar Granule Cells

  • Cho, Soon-Ok;Seong, Yeon-Hee
    • Archives of Pharmacal Research
    • /
    • v.25 no.3
    • /
    • pp.349-356
    • /
    • 2002
  • The present study was performed to examine the effect of fangchinoline, a bis- benzylisoquinoline alkaloid, which exhibits the characteristics of a $Ca^{2+}$ channel blocker, on cyanide-induced neurotoxicity using cultured rat cerebellar granule neurons. NaCN produced a concentration-dependent reduction of cell viability, which was blocked by MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, verapamil, L-type$Ca^{2+}$channel blocker, and L-NAME, a nitric oxide synthase inhibitor. Pretreatment with fangchinoline over a concentration range of 0.1 to 10 $\mu$M significantly decreased the NaCN-induced neuronal cell death, glutamate release into medium, and elevation of $[Ca^{2+}]_i$ and oxidants generation. These results suggest that fangchinoline may mitigate the harmful effects of cyanide-induced neuronal cell death by interfering with $[Ca^{2+}]_i$influx, due to its function as a $Ca^{2+}$ channel blocker, and then by inhibiting glutamate release and oxidants generation.

Synthesis of $CA_2$-based Clinker by Hydration-Burning Method (I) : Effects of Temperature on Synthesis (수화-소성법에 의한 $CA_2$클린커의 합성(I) : 합성에 미치는 온도의 영향)

  • 송태웅;한기성
    • Journal of the Korean Ceramic Society
    • /
    • v.27 no.2
    • /
    • pp.211-218
    • /
    • 1990
  • CA2-based clinker with highly activated surface and hydraulic properties was synthesized at a comparatively lowr temperature than that of conventional synthesis by "hydration-burning method". This consists of calcining the mixture of CaCO3 and Al2O3 to obtain a primary clinker, hydrating the primary clinker and reburning the hydrates to obtain final clinker. Burning of primary clinker above 1200℃ was necessary to eliminate free CaO in it and to obtain it's solid hydrate. However, rising the burning temperature above 1300℃ is ineffective due to the decrease in hydraulic properties of the primary clinker with the temperature. Hydration of primary clinker at the elevated temperature(>35℃) was required to obtain the hydrate with more porous structure and final clinker with more active surface. CA2 was formed and increased with temperature at above 1150℃, finally became a primary phase of the final clinker. However, burning at the temperature above 1300℃ resulted in reverse effect on the hydraulic properties of the final clinker due to rapid decrease in it's surface area with the temperature.

  • PDF

Characterization and Preparation of Glass-Ceramics in the System Fe_2O_3-CaO-SiO_2$ (I) (Fe_2O_3-CaO-SiO_2$계 결정화 유리의 제조 및 특성(I))

  • 이용근;최세영;김경남
    • Journal of the Korean Ceramic Society
    • /
    • v.31 no.6
    • /
    • pp.629-636
    • /
    • 1994
  • The ferrimagnetic glass-ceramics in the system Fe2O3-CaO-SiO2 for hyperthermia were investigated. Glasses could be prepared up to the content of 40 wt% of Fe2O3 and below the weight ratio of 1.0 of CaO/SiO2. The maximum saturation magnetization and the maximum coercive force were 29.85 emu/g and 340.1 Oe respectively, for a glass 40Fe2O3.20CaO.40SiO2 composition heat-treated at 95$0^{\circ}C$ for 8 hours. And for a glass 40Fe2O3.30CaO.30SiO2 composition the maximum saturation magnetization and the maximum coercive force were 18.47 emu/g and 374.4 Oe heat-treated at 1,00$0^{\circ}C$ and 90$0^{\circ}C$ for 8 hours respectively. The maximum hysteresis loss was 1,726.3 cal/g for a glass 40Fe2O3.20CaO.40SiO2 composition heat-treated at 95$0^{\circ}C$ for 8 hours. It was found that the ferrimagnetic Fe2O3.CaO.SiO2 glass-ceramics was little injurious to human body as results of biocompatibility test and biotoxicity test.

  • PDF

Cholinergic and Neurokinergic Agonist-induced $Ca^{2+}$ Responses in Rat von Ebner's Gland Acinar Cells

  • Chung, Ki-Myung;Kim, Sang-Hee;Cho, Young-Kyung;Roper, Stephen D.;Kim, Kyung-Nyun
    • International Journal of Oral Biology
    • /
    • v.31 no.3
    • /
    • pp.99-105
    • /
    • 2006
  • Von Ebner's glands (vEG) are minor salivary glands associated with circumvallate and foliate papilla. The secretions of vEG consist of microenvironment of the taste buds in the circumvallate and foliate papillae, and thus saliva from vEG plays a role in the perception of taste. The $Ca^{2+}$ signaling system in rat vEG acinar cell was examined using the $Ca^{2+}$-sensitive fluorescent indicator Fura-2. Agonist-induced increase in intracellular $Ca^{2+}\;([Ca^{2+}]_i)$ was stimulated by carbachol (CCh) and substance P (SP), but not by norepinephrine (NE), and recovered to control levels by their receptor antagonists dose-dependently. The effects were also observed in $Ca^{2+}$-free medium, suggesting mobilization from intracellular $Ca^{2+}$ store. These results in the vEG acinar cell indicate that 1) $[Ca^{2+}]_i$ is at least regulated by muscarinic and neurokininergic (NK1) receptors; 2) the increases in $[Ca^{2+}])i$ activated by CCh and SP are mainly mediated by discharge of cytosolic calcium pool.