• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.2
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• pp.408-413
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• 2007

Vascular tone plays an important role in the regulation of blood pressure. In the present study, the methanol extract of Rosae multiflora Radix (MRM) induced dose-dependent relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pretreatment of the endothelium-intact aortic tissues with $N^G$-nitro-L-arginine methly ester (L-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-${\alpha}$]-quinoxalin-1-one (ODQ) inhibited the relaxation induced by MRM, respectively. But, the relaxation effect of MRM was not blocked by indomethacine, glibenclamide, tetraethylammonium (TEA), verapamil, diltiazem, atropine, and propranolol, respectively. Moreover, incubation of endothelium-intact aortic rings with MRM increased the production of cGMP. Taken together, the present results suggest that MRM relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling. These results would be useful for further study to MRM on animal models with cardiovascular diseases.

• Journal of Chest Surgery
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• v.29 no.5
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• pp.487-494
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• 1996

The neurogenic responses of tracheal smooth muscles to electrical field stimulation (EFS) is biphasic, consisting firstly of cholinergic contraction followed by a slow and sustained relaxation. It is well known that a sustained relaxation involves the inhibitory non-adrenergic non-cholinergic systems. This study was done to Investigate the relaxing agents and their action mechanisms by use of an organ bath with plati- ilum . The tracheal smooth muscle relaxation due to EFS was suppressed by L-NAME, the WO (Nitric Oxide) synthase inhibitor, and these effects were reversed by L-arginine, the precursor of NO. Also, L-WAME (HG-nitro-L-arginine methyl ester) increased the basal tension. Nitroprusside, the NO-donor, suppressed the tracheal basal tension greatly. Methylene blue, the inhibitor of guanylate cyclase, decreased EFS-induced relaxations and increa ed basal tension. Forskolin and isoprenaline, which are activators of adenylate cyclase, suppressed tracheal basal tension in the same way as nitroprusside. TEA (tetraethylammonium), the non-specific K'channel blocker, and apamin, the Ca"-activated K'channel blocker, increased tracheal basal tension and EFS-induced relaxations. Our results indicate that Pr3 Is released upon stimulation of the NANC (Won Adrenergic Won Cholinergic) nerves in guinea-pig tracheal smooth muscle and that the release of NO related with the K+ channel, as well as the release of other inhibitory agents< e. g.)VIP (Vasoactive Intestinal Polypeptide), PHI (Peptide Histidine Isoleusine) > mediated via CAMP (cyclic Adenosine Monophosphate) may be Involved In sustained relaxation.

• Applied Chemistry for Engineering
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• v.19 no.5
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• pp.559-567
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• 2008

SAPO-34 is a well-known catalyst for methanol to olefins (MTO) process, but is rapidly deactivated by coke formation. It is necessary to improve the catalyst lifetime of SAPO-34 for MTO process. In the present work, SAPO-34 catalysts were synthesized with a variety of structure directing agent, and the physicochemical properties of the catalysts were examined by $N_2$-isotherm, XRD, SEM, and $NH_3$-TPD. It was found that mixed structure directing agents, especially DEA and TEAOH, gave well developed SAPO-34 crystal structure and reduced the crystal size and moderated acidity of SAPO-34 under the same synthetic conditions as that of various structure directing agents. Also, we could find that SAPO-34 catalyst prepared by mixed templates of DEA and TEAOH had the superior catalytic activity and the longer lifetime in MTO reaction.

• The Korean Journal of Physiology and Pharmacology
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• v.3 no.1
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• pp.1-10
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• 1999

We sought to find out the mechanism of vascular relaxation by extracellular $K^+$ concentration $([K^+]_o)$ in the cerebral resistant arteriole from rabbit. Single cells were isolated from the cerebral resistant arteriole, and using voltage-clamp technique barium-sensitive $K^+$ currents were recorded, and their characteristics were observed. Afterwards, the changes in membrane potential and currents through the membrane caused by the change in $[K^+]_o$ was observed. In the smooth muscle cells of cerebral resistant arteriole, ion currents that are blocked by barium, 4-aminopyridine (4-AP), and tetraethylammonium (TEA) exist. Currents that were blocked by barium showed inward rectification. When the $[K^+]_o$ were 6, 20, 60, and 140 mM, the reversal potentials were $-82.7{\pm}1.0,\;-49.5{\pm}1.86,\;-26{\pm}1.14,\;-5.18{\pm}1.17$ mV, respectively, and these values were almost identical to the calculated $K^+$ equilibrium potential. The inhibition of barium-sensitive inward currents by barium depended on the membrane potential. At the membrane potentials of -140, -100, and -60 mV, $K_d$ values were 0.44, 1.19, and 4.82 ${\mu}M,$ respectively. When $[K^+]_o$ was elevatedfrom 6 mM to 15 mM, membrane potential hyperpolarized to -50 mV from -40 mV. Hyperpolarization by $K^+$ was inhibited by barium but not by ouabain. When the membrane potential was held at resting membrane potential and the $[K^+]_o$ was elevated from 6 mM to 15 mM, outward currents increased; when elevated to 25 mM, inward currents increased. Fixing the membrane potential at resting membrane potential and comparing the barium-sensitive outward currents at $[K^+]_o$ of 6 and 15 mM showed that the barium- sensitive outward current increased at 15 mM $K^+.$ From the above results the following were concluded. Barium-sensitive $K^+$?channel activity increased when $[K^+]_o$ is elevated and this leads to an increase in $K^+-outward$ current. Consequently, the membrane potential hyperpolarizes, leading to the relaxation of resistant arteries, and this is thought to contribute to an increase in the local blood flow of brain.

• Journal of Ginseng Research
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• v.23 no.4
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• pp.230-234
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• 1999

Potassium channels play an important role in regulating vascular smooth muscle tone. Four types of $K^+$ channels areknown to be expressed in vascular smooth muscle cells, and maxi $Ca^{2+}-activated\;K^+$ channel $(BK_{Ca})$ is a dominant type of $K^+$ channels in these cells. Because total ginseng saponins and ginsenoside $Rg_3$ cause vasodilation with unclear mechanisms, we hypothesized that total ginseng saponins and ginsenoside $Rg_3$ induce vasodilation via activation of maxi $Ca^{2+}-activated\;K+$ channels. Whole-cell BKe. currents were voltage-dependent with half maximum activation at -14 mV, and the currents were sensitive to nanomolar ChTX and millimolar TEA. External application of total ginseng saponins increased the anlplitude of the whole-cell BKe. current in a concentration-dependent manner. Single-channel analysis indicates that total ginseng saponins caused the channel opening for a longer period of time. Ginsenoside $Rg_3$ increased the amplitude of whole-cell $K_{Ca}$ currents without affecting voltage dependence of the currents and increased single-channel open time. Hence, the results suggest that ginseng saponin-induced vasodilation may be due to activation of $K_{Ca}$.

• Journal of Ginseng Research
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• v.26 no.1
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• pp.1-5
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• 2002

It has been well known that Korea red ginseng has an antihypertensive effect. The antihypertensive effect may be due to its ability to change the peripheral resistance. Change of vascular tone in the resistance-sized artery contribute to the peripheral resistance, thereby regulate the blood pressure. Therefore, we investigated to clarify the vasorelaxing mechanism induced by crude saponin of Korea red ginseng in the resistance-sized mesenteric artery of rats. The resistance-sized mesenteric artery was isolated and cut into a ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured using myograph force-displacement transducer. Crude saponin of ginseng relaxed the mesenmetric arterial rings precontracted with norepinephrine (3$\mu$M) in dose-dependent manner (0.01 mg/㎖ -1 mg/㎖. The relaxation by crude saponin was smaller in endothelium-intact preparation than that in endothelium-denuded preparation. The contraction induced by A23187 or phorbol 12,13-dibutyrate was not affected by crude saponin of ginseng. The vasorelaxing effect of crude saponin of ginseng was significantly attenuated by the increase of the extracellular K$\^$+/ concentration. Crude saponin-induced vasorelaxation was not affected by tetraethylammonium (1 mM), glybenclamide (10$\mu$M), and 4-aminopyridine (0.1 mM) in these preparations. Ba$\^$2+/(10$\mu$M ∼100$\mu$M) markedly reduced the crude saponin-induced vasorelakation dose-dependently. From the above results, we suggest that crude saponin of ginseng may stimulate K$\^$+/ efflux and hyperpolarize the membrane, thereby cause the vasorelaxation in the resistance-sized mesenteric artery of rats.

• Journal of Physiology & Pathology in Korean Medicine
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• v.33 no.4
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• pp.198-206
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• 2019

This study was conducted to evaluate the vasorelaxant effect of DangGuiSu-San and SamHwangSaSim-Tang extract on contracted rabbit carotid artery. To study the effect of DangGuiSu-San and SamHwangSaSim-Tang extract on contracted rabbit carotid arterial strips, arterial strips with intact or damaged endothelium were used for experiment using organ bath. The pre-contracted arterial strips with Phenylephrine(PE) was treated with various concentrations of DangGuiSu-San and SamHwangSaSim-Tang extract(0.01, 0.03, 0.1, 0.3 and $1.0mg/m{\ell}$). To determine the mechanisms of DangGuiSu-San and SamHwangSaSim-Tang-induced vasorelaxant, DangGuiSu-San and SamHwangSaSim-Tang extract were infused into contracted arterial rings which had been pretreated by indomethacin(IM), tetraethylammonium chloride(TEA), $N{\omega}$-nitro-L-arginine ($_L-NNA$), methylene blue(MB). And calcium chloride(Ca) 1 mM was infused into precontracted arterial ring induced by PE after treatment of DangGuiSu-San and SamHwangSaSim-Tang extract in $Ca^{2+}$-free krebs solution. DangGuiSu-San and SamHwangSaSim-Tang extract revealed significant relaxation on PE-induced arterial contraction. DangGuiSu-San and SamHwangSaSim-Tang extract also had an effective relaxation to the intact endothelium arterial ring. SamHwangSaSim-Tang extract on contracted rabbit carotid artery is related with NO-cGMP pathway. Pretreatment of DangGuiSu-San and SamHwangSaSim-Tang extract inhibited the contraction by influx of extracellular $Ca^{2+}$ in contracted arterial ring induced by NE. This study indicated that the relaxation effect of SamHwangSaSim-Tang extract on contracted rabbit carotid artery is related with NO-cGMP pathway. Pretreatment of DangGuiSu-San and SamHwangSaSim-Tang extract inhibited the contraction by influx of extracellular $Ca^{2+}$ in contracted arterial ring induced by NE.

• The Korea Journal of Herbology
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• v.28 no.4
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• pp.63-69
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• 2013

Objectives : The purpose of present study was to investigate the vasorelaxant activities and mechanisms of action of the ethanol extract of P. yedoensis leaf (PYL) on isolated rat aortic rings. Methods : Dried P. yedoensis leaves were extracted 3 times with 100% ethanol for 3 h in a reflux apparatus. Isolated rat aortic rings were suspended in organ chambers containing 10 ml Krebs-Henseleit (K-H) solution. The rings were maintained at $37^{\circ}C$ and aerated with a mixture of 95% $O_2$ and 5% $CO_2$. Changes in their tension were recorded via isometric transducers connected to a data acquisition system. Results : PYL relaxed the contraction of aortic rings induced by phenylephrine (PE, 1 ${\mu}M$) or KCl (60 mM) in a concentration dependent manner. However, the vasorelaxant effects of PYL on endothelium-denuded aortic rings were lower than endothelium-intact aortic rings. And the vasorelaxant effects of PYL on endothelium-intact aortic rings were reduced by pre-treatment with $N{\omega}$-Nitro-L-arginine methyl ester (10 ${\mu}M$), methylene blue (10 ${\mu}M$), 1-H-[1,2,4]-oxadiazolo-[4,3-${\alpha}$]-quinoxalin-1-one (10 ${\mu}M$), tetraethylammonium (5 mM). In addition, PYL inhibited the contraction induced by extracellular $Ca^{2+}$ in endothelium-denuded aortic rings pre-contracted by PE or KCl in $Ca^{2+}$-free K-H solution. Conclusions : These results suggest that PYL exerts its vasorelaxant effects via the activation of Nitric Oxide (NO) formation by means of L-arginine and NO-cGMP pathways and via the blockage of receptor operated calcium channels, voltage dependent calcium channels and calcium-activated potassium channels.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.301-309
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• 1996

Since it has been reported that the depolarization-induced NE release is inhibited by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic $A_1-adenosine$ receptor on the NE release has not been clearly elucidated yet. Therefore, it was attempted to clarify the participation of $K^+-channel$ in the post-receptor mechanisms of the $A_1-adenosine$ receptor-mediated control of NE release in this study. Slices from rat hippocampus were equilibrated with $^3H-norepinephrine$ and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 $VCm^{-1}$, 2 ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from $1{\sim}30\;{\mu}M$, decreased the NE release in a dose-dependent manner, without affecting the basal rate of release. 4AP $(1{\sim}30{\mu}M)$, a specific A-type $K^+-channel$ blocker, increased the evoked NE release in a dose-related fashion, and the basal rate of release is increased by 10 and $30{\mu}M$. TEA $(1{\sim}10{\mu}\;M)$, a nonspecific $K^+-channel$ blocker, increased the evoked NE release in a dose-dependent manner without affecting basal release. The adenosine effects were significantly inhibites by 3 ${\mu}M$ 4AP and 10 mM TEA treatment. 4AP $(30{\mu}M)-$ and TEA (10 mM)-induced increments of evoked NE release were completely abolished in $Ca^{++} free, but these were recoverd in low $Ca^{++} medium. And the effects of $K^+-channel$ blockers in low $Ca^{++} medium were inhibites and abolishes by $Mg^{++} (4 mM) adding and TTX $(0.3{\mu}M)$ adding medium, respectively. These results suggest that the decrement of the evoked NE-release by $A_1-adenosine$ receptor is mediated by 4AP and TEA sensitive $K^+-channel$.

• Journal of Chest Surgery
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• v.42 no.5
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• pp.588-596
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• 2009

Background: To clarify the effect of hypoxia on vascular contractility, we tried to show whether hypoxia induced the release of endothelium-derived relaxing factor (EDRF) and the nature of the underlying mechanism for this release. Material and Method: Isometric contractions were observed in rabbit aorta, and the released EDRF from the rabbit aorta was bioassayed by using rabbit denuded carotid artery. The intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in the cultured rabbit aortic endothelial cells was recorded by a microfluorimeter with using Fura-2/AM. Hypoxia was evoked to the blood vessels or endothelial cells by eliminating the $O_2$ in the aerating gases in the external solution. Chemical hypoxia was evoked by applying deoxyglucose or $CN^-$. Result: Hypoxia relaxed the precontracted rabbit thoracic aorta that had its endothelium, and the magnitude of the relaxation was gradually increased by repetitive bouts of hypoxia. In contrast, hypoxia-induced relaxation was not evoked in the aorta that was denuded of endothelium. In a bioassay experiment, hypoxia released endothelium-derived relaxing factor (EDRF) and the release was inhibited by L-NAME or the $K^+$ channel blocker tetraethylammonium (TEA). In the cultured endothelial cells, hypoxia augmented the ATP-induced increase of the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) and this increase was inhibited by TEA. Furthermore, chemical hypoxia also increased the $Ca^{2+}$ influx. Conclusion: From these results, it can be concluded that hypoxia might induce the release of NO from rabbit aortic endothelial cells by increasing $[[Ca^{2+}]_i$.