• 약학회지
• /
• 제55권2호
• /
• pp.168-171
• /
• 2011

Chrysosplenol C [5,6-dihydroxy-2-(4-hydroxy-3-methoxyphenyl)-3,7-dimethoxychromen-4-one] is a flavonoid found in Miliusa balansae and Pterocaulon sphacelatum. We have recently shown that chrysosplenol C has positive inotropic effect in isolated rat ventricular myocytes. In the present study, we explored a possible mechanism for the positive inotropic effect of chrysosplenol C by examining intracellular $Ca^{2+}$ transients during action potentials. The intracellular $Ca^{2+}$ transients were measured by confocal $Ca^{2+}$ imaging in field-stimulated single rat ventricular myocytes. Chrysosplenol C (50 ${\mu}M$) significantly increased the magnitudes (${\Delta}F/F_0$) of $Ca^{2+}$ transients (control, $1.08{\pm}0.05$; chrysosplenol C, $1.25{\pm}0.03$; n=8, P<0.01). Half decay time of the action potential-induced $Ca^{2+}$ transient was not altered by chrysosplenol C (50 ${\mu}M$) (control, $154{\pm}6$ ms; chrysosplenol C, $167{\pm}11$ ms; n=21). The $Ca^{2+}$ content in the sarcoplasmic reticulum (SR), measured as caffeine (10 mM)-induced $Ca^{2+}$ transient, was significantly decreased by chrysosplenol C (50 ${\mu}M$). These results indicate that chrysosplenol C increases $Ca^{2+}$ transients without altering $Ca^{2+}$ removal kinetics in ventricular myocytes, providing a possible mechanism for its positive inotropic effect.

• 대한한방내과학회지
• /
• 제21권3호
• /
• pp.377-388
• /
• 2000

Objective : This study was undertaken to evaluate the effect of Sunghyangchungisan (SHCS) on the regulation of vascular tone and $Ca^{2+}$ metabolism in arterial tissues. Vascular rings isolated from rabbit carotid artery were myographed isometrically in isolated organ baths and the effect of SHCS on contractile activities, endothelial function and $Ca^{2+}$ metabolism were determined. Methods : In phentobarbital sodium-anesthetized rabbits, SHCS administered through ear vein (100 mg/Kg body wt.) or intragastric dwelling tube (300 mg/Kg body wt.) attenuated phenylephrine (PE, 10 ${\mu}g$/Kg, i.v.)-induced increases in both systolic and diastolic cartoid arterial blood pressure. Results : In experiments with isolated arterial strips, SHCS relaxed arterial rings which were pre-contracted by phenylephrine (PE, 1 ${\mu}M$). The responses to SHCS were partially dose-dependent at concentrations lower than 0.5 mg/ml. When SHCS was applied prior to the exposure to PE, it inhibited the PE-induced contraction by a similar magnitude which was comparable to the relaxation of pre-contracted arterial rings. Washout of SHCS after observing its relaxant effect resulted in a full recovery of PE-induced contractions, indicating that the action mechanism is reversible. The observation that SHCS did not change the $ED_{50)$ of PE oh its dose-response curve ruled out the possible interaction of SHCS with ${\alpha}$-receptors. The relaxant effect of SHCS was not affected by removal of endothelium or a nitric oxide synthase inhibitor, L-NAME. Methylene blue, an inhibitor of the soluble guanylate cyclase, did not affect the relaxant effect of SHCS. These results suggest that the action of SHCS is not mediated by the endothelium nor soluble guanylate cyclase. Constant cGMP production determined in arterial strips in the presence or absence of SHCS is consistent with this conclusion. When contraction was induced by additive application of $Ca^{2+}$ in arterial rings which were pre-depolarized by high $K^+$ in a $Ca^{2+}$-free solution, the relaxant effect of SHCS was attenuated by increasing the $Ca^{2+}$ concentration. SHCS, when applied to the arterial rings pre-contracted by PE and then relaxed by nifedipine, a $Ca^{2+}$ channel blocker, did not show additive relaxation. SHCS partially blocked $Ca^{2+}$ influx stimulated by PE and high $K^+$ which was determined by 5-min ^{45}Ca$ uptake, while it did not affect $Ca^{2+}$ efflux. Conclusions : From above results, it is suggested that SHCS relax PE-induced contraction of rabbit carotid artery in an endothelium independent manner, andinhibition of $Ca^{2+}$ influx may contribute to the underling mechanism.

• The Korean Journal of Physiology and Pharmacology
• /
• 제1권5호
• /
• pp.485-493
• /
• 1997

We investigated the effect of ${\alpha}-adrenergic$ and cholinergic receptor agonists on $Ca^{2+}$ current in adult rat trigeminal ganglion neurons using whole-cell patch clamp methods. The application of acetylcholine, carbachol, and oxotremorine ($50\;{\mu}M\;each$) produced a rapid and reversible reduction of the $Ca^{2+}$ current by $17{\pm}6%,\;19{\pm}3%,\;and\;18{\pm}4%$, respectively. Atropine, a muscarinic antagonist, blocked carbachol- induced $Ca^{2+}$ current inhibition to $3{\pm}1%$. Norepinephrine ($50\;{\mu}M$) reduced $Ca^{2+}$ current by $18{\pm}2%$, while clonidine ($50\;{\mu}M$), an ${\alpha}2-adrenergic$ receptor agonist, inhibited $Ca^{2+}$ current by only $4{\pm}1%$. Yohimbine, an ${\alpha}2-adrenergic$ receptor antagonist, did not block the inhibitory effect of norepinephrine on $Ca^{2+}$ current, whereas prazosin, an ${\alpha}1-adrenergic$ receptor antagonist, attenuated the inhibitory effect of norepinephrine on $Ca^{2+}$ current to $6{\pm}1%$. This pharmacology contrasts with ${\alpha}2-adrenergic$ receptor modulation of $Ca^{2+}$ channels in rat sympathetic neurons, which is sensitive to clonidine and blocked by yohimbine. Our data suggest that the modulation of voltage dependent $Ca^{2+}$ channel by norepinephrine is mediated via an α1-adrenergic receptor. Pretreatment with pertussis toxin (250 ng/ml) for 16 h greatly reduced norepinephrine- and carbachol-induced $Ca^{2+}$ current inhibition from $17{\pm}3%\;and\;18{\pm}3%\;to\;2{\pm}1%\;and\;2{\pm}1%$, respectively. These results demonstrate that norepinephrine, through an ${\alpha}1-adrenergic$ receptor, and carbachol, through a muscarinic receptor, inhibit $Ca^{2+}$ currents in adult rat trigeminal ganglion neurons via pertussis toxin sensitive GTP-binding proteins.

• 한국콘크리트학회:학술대회논문집
• /
• 한국콘크리트학회 2005년도 봄학술 발표회 논문집(II)
• /
• pp.349-352
• /
• 2005

In this work, effects of limestone powder on hydration of $C_3A-CaSO_4\cdot2H_2O$ system was discussed based on the XRD Quantitative analysis, and the possibility of Delayed Ettringite Formation was also discussed. The early hydration of $C_{3}A$ was delayed by addition of $CaCO_{3}$ powder. The delay effect was enhanced by increasing of $CaCO_{3}$ content and finer powder of $CaCO_{3}$ addition. After consumption of $CaSO_4\cdot2H_2O$, the reaction of $CaCO_{3}$ is started. Delayed Ettringite Formation would take place because monosulfoaluminate is not stable in presence of $CaCO_{3}$. In order to prevent the delayed ettringite formation in $C_3A-CaSO_4\cdot2H_2O-CaCo_3$ system, the reduction of monosulfoaluminate formation is important. Therefore, by increasing the amount of $CaCO_{3}$ addition and finer $CaCO_{3}$ powder addition, the delayed ettringite formation can be prevented.

• 한국세라믹학회지
• /
• 제32권9호
• /
• pp.1033-1039
• /
• 1995

The current experiment has quantitatively investigated the effect of the content of CaO and SiO2 on the microstructure, density, electrical resistivity, power loss and initial permeability of manganese zinc ferrites. The density increased initially with CaO and SiO2 content and the further addition showed an adverse effect. The excess addition of CaO and SiO2 developed a discontinuous grain growth with numerous pores inside grains and lowered the electrical resistivity. The initial permeability decreased with increasing the content of SiO2. The samples with relatively low power loss showed that half of the total loss at 10$0^{\circ}C$, 100 kHz and 2000 Gauss was due to the eddy current loss.

• The Korean Journal of Physiology
• /
• 제11권2호
• /
• pp.9-16
• /
• 1977

The present experiment was conducted to see whether or not several cardioactive agents influence the 'regenerative $Ca^{++}$ release' in the mechanically disrupted cardiac cells. The mechanically disrupted cardiac cells were prepared by the method of Kerrick and Best from the ventricle of rat. The tension development of the disrupted cardiac cells was measured with a mechanoelectric transducer (RCA 5734). The results were summarized as follows 1) 2 mM caffeine enhanced the regenerative $Ca^{++}$ release, whereas 2 mM Procaine inhibited the $Ca^{++}$ release as reported by other investigators. 2) Epinephrine at concentrations of $10^{-7},\;10^{-6}\;and\;10^{-5}M$ increased the regenerative $Ca^{++}$ release significantly but showed a poor dose response on the $Ca^{++}$ release. 3) Propranolol showed no effect on the regenerative $Ca^{++}$ release when studied alone. Furthermore, it showed no antagonistic effect on an increased regenerative $Ca^{++}$ release induced by epinephrine. 4) Other cardioactive agents such as acetylcholine, ouabain, isoproterenol and c-AMP at concentrations of $10^{-6}M$ showed no effect on the regenerative $Ca^{++}$ release. From the above results, it may be concluded that the cardioactive actions of these agents are not related directly to the process of regenerative $Ca^{++}$ release.

• The Korean Journal of Physiology and Pharmacology
• /
• 제19권5호
• /
• pp.413-420
• /
• 2015

Dexmedetomidine is a sedative and analgesic agent that exerts its effects by selectively agonizing ${\alpha}2$ adrenoceptor. Histamine is a pathophysiological amine that activates G protein-coupled receptors, to induce $Ca^{2+}$ release and subsequent mediate or progress inflammation. Dexmedetomidine has been reported to exert inhibitory effect on inflammation both in vitro and in vivo studies. However, it is unclear that dexmedetomidine modulates histamine-induced signaling and pro-inflammatory cytokine expression. This study was carried out to assess how dexmedetomidine modulates histamine-induced $Ca^{2+}$ signaling and regulates the expression of pro-inflammatory cytokine genes encoding interleukin (IL)-6 and -8. To elucidate the regulatory role of dexmedetomidine on histamine signaling, HeLa cells and human salivary gland cells which are endogenously expressed histamine 1 receptor were used. Dexmedetomidine itself did not trigger $Ca^{2+}$ peak or increase in the presence or absence of external $Ca^{2+}$. When cells were stimulated with histamine after pretreatment with various concentrations of dexmedetomidine, we observed inhibited histamine-induced $[Ca^{2+}]_i$ signal in both cell types. Histamine stimulated IL-6 mRNA expression not IL-8 mRNA within 2 hrs, however this effect was attenuated by dexmedetomidine. Collectively, these findings suggest that dexmedetomidine modulates histamine-induced $Ca^{2+}$ signaling and IL-6 expression and will be useful for understanding the antagonistic properties of dexmedetomidine on histamine-induced signaling beyond its sedative effect.

• 원예과학기술지
• /
• 제16권2호
• /
• pp.215-218
• /
• 1998

참외 '금싸라기은천'의 이상 발효과 발생억제에 미치는 $CaCl_2$의 엽면처리 효과를 실험하였다. $CaCl_2$(0.3~0.7%)를 개화후 10일부터 5일간격으로 3회 엽면처리하므로써 발효과 발생이 현저히 억제되었으며 유효농도는 0.3~0.5%였다. 과실성숙기의 관수는 $CaCl_2$효과를 감소시켰다. 당함량은 정상과가 발효과에 비하여 높았고 $CaCl_2$처리는 당함량에 영향을 미치지 않았다. 과실내 Ca함량은 정상과가 발효과 보다 높았으나 K와 Mg함량은 차이가 없었다. 질소시용량이 적든가(10kg/10a) 또는 많으면 (25kg/10a) 발효과 발생이 많았으나 질소시용량은 과실내 Ca함량에 영향을 미치지 않았다.

• 대한약리학회지
• /
• 제27권1호
• /
• pp.53-67
• /
• 1991

흰쥐 적출 부신에서 DMPP와 McN-A-343의 카테콜아민(CA) 분비작용의 차이와 특성에 대해서 연구한 결과 다음과 같다. DMPP(100 uM)와 McN-A-343(100 uM)은 부신정맥내로 투여시 유의한 카테콜아민 분비작용을 나타내었다. Mol농도로 비교시 McN-A-343의 CA분비작용은 DMPP의 약 1/5정도였다. DMPP나 McN-A-343의 반복투여시 반응 급강현상은 관찰할 수 없었다. DMPP의 CA분비작용은 chlorisondamine이나 desipramine또는 $Ca^{2+}-free$ Krebs + EGTA 관류등의 전처치로 의의있게 억제되었으나, pirenzepine, ouabain 및 physostigmine등 전처치에 의해서는 영향을 받지 않았다. 그러나 atropine 전처치시 DMPP의 분비작용은 오히려 증강되었다. McN-A-343의 CA분비작용은 atropine, pirenzepine, chloriondamine, physostigmine 및 $Ca^{2+}-free$ medium plus EGTA 관류등의 전처치에 의해서현처히 차단되었으나 desipramine등에 의해서는 영향을 받지 않았다. 그러나 ouabain의 전치치시 McN-A-343의 분비효과는 크게 증강되었다. 이상의 실험결과로 보아 DMPP와 McN-A-343은 횐쥐 적출관류 부신에서 현저한 CA분비작용을 일으키며, 이는 $Ca^{2+}$ 의존성 임을 보였으며, DMPP의 분비작용은 부신의 nicotine 수용체의 흥분을 통해서 나타내며, 또한 McN-A-343의 분비작용은 $M_{1}-muscarine$ 수용체의 흥분에 의하여 유발되는 것을 생각된다. DMPP의 분비활성이 McN-A-343보다 훨씬 강력한 것으로 사료된다.

• Restorative Dentistry and Endodontics
• /
• 제39권4호
• /
• pp.241-252
• /
• 2014

The goal of endodontic treatment is the prevention and control of pulpal and periradicular infections. Calcium hydroxide ($Ca(OH)_2$) has been widely used in endodontics as an intracanal medicament to eliminate the remaining microorganisms after chemomechanical preparation. The purpose of this article is to review the antimicrobial properties of $Ca(OH)_2$ as an intracanal medicament in root canal treatment. The first part of this review details the characteristics of $Ca(OH)_2$ and summarizes the results of in vitro studies related to its antimicrobial effect. The antimicrobial effect of $Ca(OH)_2$ results from the release of hydroxyl ions when it comes into contact with aqueous fluids. $Ca(OH)_2$ has a wide range of antimicrobial effects against common endodontic pathogens, but is less effective against Enterococcus faecalis and Candida albicans. The addition of vehicles or other agents might contribute to the antimicrobial effect of $Ca(OH)_2$.