• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.145-152
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• 1990

We recently reported a development of an experimental system which can identify the release of a superoxide-dependent vasorelaxant factor from endothelial cells using a two-bath system. In the present work, we further exploited the above system and observed whether the superoxide-dependent relaxing factor(s), released from the porcine coronary artery (PCA) endothelium, was similar in relaxation to those obtained from cat thoracic aortic endothelium and cultured endothelial cells of bovine aorta. However, there was observed a novel difference among the former one and the latter two relaxing factors; the release of relaxing factor from PCA endothelium can be inhibited either by catalase or by superoxide dismutase (SOD), whereas the latter two can be inhibited only by SOD. It was further attempted to characterize the synthetic mechanisms of the relaxing factors: (1) They were readily inhibited by various lipoxygenase inhibitors (gossypol, nordihydroguaiaretic acid, AA 861, and eicosatetraynoic acid). (2) They were not inhibited by cyclooxygenase inhibitor (indomethacin) and by cytochrome P-450 monooxygenease inhibitors (proadifen and cimetidine). Thus, it is likely that these relaxing factors, although obtained from different species, show common functional roles of arteriolar relaxation. It is suggested that they are related to pathophysiological involvement of various tissue ischemia-reperfusion injuries.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1993.11a
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• pp.36-38
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• 1993

내피세포 (endothelial cells, EC)는 amine, peptide, 단백, arachidonic acid 및 그 대사물 등의 여러 화학물질에 의하여 내피세포 의전성 이완물질 endothelium-derived relaxing factor, EDRF)을 유리할 뿐만 아니라 맥압(脈壓)과 같은 물리적 변동에 의하여서도 EDRF가 유리된다. EDRF는 처음에 Furchgott와 Zawadzki (1980)에 의하여 보고되었고, EDRF의 실질적인 성분이 무엇인가에 대하여는 그동안 많이 검토되어 왔다(Marshall 와 Kontos, Hong 등, 1990).Ignarro 등 (1987)과 Palmer등 (1987)은 EDRF에 의한 생물학적 반응이 NO (nitric oxide)와 유사하거나 같은 물질이라고 보고하였고,Furchgott 등 (1986)과 Ignarro등 (1988)도 EDRF가 NO와 유사하거나 같은 물질일 것이라고 단정하였다.

• The Journal of Korean Medicine
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• v.19 no.2
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• pp.50-58
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• 1998

The effects of the Evodiae fructus on the cardiovascular function were assessed in spontaneously hypertensive rats, and isolated preparation of spontaneously hypertensive rats aortic strip. In spontaneously hypertensive rats, intraperitoneal administration of methanol crude extract of Evodiae Fructus (0.5mg/kg) lowered aterial blood pressure which lasted for at least 4 hours. The hypotensive effect of Evodiae Fructus was more stronger with ${\alpha}-adrenoreceptor$ inhibitor(Phentholamine) and it was not affected by ${\beta}-adrenoreceptor$ inhibitor(Propranolol). The hypotensive effect of Evodiae Fructus was abolished by NAME. It is suggested that the hypotensive effect of Evodiae Fructus may be concern with endothelium-derived relaxing factor and it may be mediated through NO synthesis. Evodiae Fructus showed a vasorelaxing effect on denude aortic strip. It is suggested that Evodiae Fructus has a direct relaxing effect on vascular smooth muscle cells. Judging from above results, it was proved that hypotensive effect of Evodiae Fructus. The mechanism of hypotensive action may be concern with endothelium-derived relaxing factor and direct relaxing effect on vascular smooth muscle cells. Therefore, it is suggested that Evodiae Fructus is applicable to hypertension.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.27-37
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• 1995

In anesthetized rats, we examined the possibility that endothelium-derived relaxing factor (EDRF) or nitric oxide (NO) released in response to cholinergic mechanism may contribute to the reflex autoregulation of cerebral blood flow. Suffusion with mock cerebrospinal fluid (CSF), containing acetylcholine (ACh, $10^{-9}{\sim}10^{-6}M$) evoked concentration-dependent vasodilatation of the resting pial artery (mean, $19.3{\pm}1.7{\mu}m$, n=36), which was significantly inhibited not only by $N{\omega}$-nitro-L-arginine (L-NNA, $10^{-5}M$) but also by methylene blue ($10^{-6}M$) and oxyhemoglobin ($10^{-6}M$). The muscarinic receptors in the endothelium of pial artery implicated in the release of EDRF were considered to be $M_1\;and\;M_3$ subtypes. When suffused with mock CSF containing L-arginine it caused a transient vasodilatation, which was strongly inhibited by LY 83583 ($10^{-5}M$), but not by L-NNA ($10^{-5}M$). Additionally, both ACh- and L-arginine-induced vasodilation were significantly inhibited by glibenclamide, a specific ATP-sensitive $K^+$ channel blocker. On the other hand, changes in pial arterial diameter were plotted as a function of changes in systemic arterial blood pressure. The slopes of regression lines for vasodilation and vasoconstriction were not affected by pretreatment with $10^{-5}M$ L-NNA, but significantly reduced by $3{\times}10^{-6}M$ glibenclamide. Thus it is suggested that the reflex vasodilation of rat pial arteries in response to a transient hypotension is not mediated by EDRF (NO).

• Toxicological Research
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• v.30 no.3
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• pp.141-148
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• 2014

Endothelium-derived relaxing factors (EDRFs), including nitric oxide (NO), prostacyclin ($PGI_2$), and endothelium-derived hyperpolarizing factor (EDHF), play pivotal roles in regulating vascular tone. Reduced EDRFs cause impaired endothelium-dependent vasorelaxation, or endothelial dysfunction. Impaired endothelium-dependent vasorelaxation in response to acetylcholine (ACh) is consistently observed in conduit vessels in human patients and experimental animal models of hypertension. Because small resistance arteries are known to produce more than one type of EDRF, the mechanism(s) mediating endothelium-dependent vasorelaxation in small resistance arteries may be different from that observed in conduit vessels under hypertensive conditions, where vasorelaxation is mainly dependent on NO. EDHF has been described as one of the principal mediators of endothelium-dependent vasorelaxation in small resistance arteries in normotensive animals. Furthermore, EDHF appears to become the predominant endothelium-dependent vasorelaxation pathway when the endothelial NO synthase (NOS3)/NO pathway is absent, as in NOS3-knockout mice, whereas some studies have shown that the EDHF pathway is dysfunctional in experimental models of hypertension. This article reviews our current knowledge regarding EDRFs in small arteries under normotensive and hypertensive conditions.

• Proceedings of the Ginseng society Conference
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• 1993.09a
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• pp.40-48
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• 1993

Intravenous administration of saponin extracted from the root of Panax ginseng lowered the blood pressure dose-dependently (10-200 mg/kg, B.W) in anesthetized rats. Therefore, experiments were designed to study the hypothesis that the lowering of blood pressure is associated with the release of endothelium-derived relaxing factor and the accumulation of guanosine 3, 5-cyclic monophosphate (cGMP). Rings of thoracic aorta with and without endothelium were suspended for the measurement of isometric tension in organ chamber and the tissue content of cGMP was measured by radioimmunoassay. All experiments were performed in the presence of $indomethacin(10^{-5}M).$ Ginseng saponin $(10^{-5}-3{\times}10^{-6}g/ml)$ relaxed contractions induced by phenylephrine $10^{-6}M)$ in the aorta with endothelium but not in that without endothelium. Treatment of aortic rings with $N^G$ monomethyl-L-arginine (L-NMMA, $10^{-4}M$ for 30 min), a competitive inhibitor of nitric oxide synthase, and methylene blue $(MB,\;3{\times}10^{-7}M$ for 30 min). an inhibitor of soluble guanylate cyclase, diminished the relaxation induced by Ginseng saponin. Ginseng saponin $10^{-4}g/ml$ for 2 min) increased the accumulation of cGMP in rings with endothelium. L-NMMA and MB inhibited the accumulation of cGMP induced by Ginseng saponin. These data suggest that vascular relaxations induced by Ginseng saponin are mediated by release of endothelium-derived relaxing factor and the accumulation of cGMP. The effect of Ginseng saponin on endothelial function in hypercholesterolemic rabbits was examined. In hypercholesterolemic rabbits fed with $2\%$ cholesterol for 8 weeks, relaxation of aortic rings to acetylcholine was impaired. The impaired relaxations of aortic rings in hypercholesterolemic rabbits were improved by dietary supplementation of Ginseng saponin, probably because of an improved release of endothelium - derived relaxing factor.

• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.125-133
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• 1991

In the isolated rabbit mesenteric artery denuded of endothelium, we characterized the identity of the A23187-induced endothelium-dependent relaxing factor (EDRF) released from the endothelium of rabbit aorta, which is distinct from that of acetylcholine-induced relaxing factor. In the normal physiological salt solution (PSS), the dose-response curves to A23187 and acetylcholine were overlapped together. Their effects were also inhibited by methylene blue. Upon application of hypoxanthine and xanthine oxidase into the bath, the phenylephrine-induced precontraction was transiently increased followed by the sustained relaxation. During the burst of hypoxanthine-xanthine oxidase reaction, the $Ca^{++}$ ionophore, A23187 but not acetylcholine was able to cause an immediate relaxation. However, A23187-induced relaxation was not manifested when precontracted by 50 mM $K^+-PSS$. Nevertheless, in the presence of superoxide dismutase, A23187 could produce an immediate relaxation without accompanying the transient contraction as acetylcholine did during the hypoxanthine-xanthine oxidase reaction. On the other hand, acetylcholine-induced relaxation was more sensitively inhibited by phorbol 12-myristate 13-acetate (PMA) than A23187-induced relaxation. Endothelium-independent relaxation to sodium nitroprusside was not affected by PMA. Based on these results it is suggested that both A23187 and acetylcholine cause the methylene blue-inhibitable endothelium-dependent relaxation, and in addition, A23187 may release a stable EDRF which is resistant to superoxide anion and PMA.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.6
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• pp.809-817
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• 2013

The aim of this study was to evaluate the mechanism of vasodilation of Lespedezea cuneata(LC) in rabbit common carotid artery and cavernosal smooth muscle. LC relaxed arterial strips precontracted with norepinephrine and cavernosal strips precontracted with phenylephrine. The arterial relaxation effects of LC was endothelium-dependent. $N{\omega}$-nitro-L-arginine(L-NNA), NOS inhibitor, methylene blue(MB), cGMP inhibitor, indomethacin(IM), cyclo-oxygenase inhibitor and tetraethylammonium chloride(TEA), KCa-channel blocker attenuate the relaxation responses of LC in arterial strips. In $Ca^{2+}$-free krebs-ringer solution, pretreatment of LC extract significantly reduced the contraction induced by addition $Ca^{2+}$. L-NNA reduced LC extract-induced relaxation in cavernosal strips, but IM, TEA and MB didn't affect LC extract-induced relaxation. When LC extract was applicated on human umbilical vein endothelial cell, the nitric oxide concentration was increased. We conclude that in rabbit common carotid artery, LC may suppress influx of extra-cellular $Ca^{2+}$ through the release of endothelium derived relaxing factor including nitric oxide, prostacyclin, endothelium derived hyperpolarizing factor. And LC exerts a relaxing effect on corpus cavernosum through activating the NO.

• Journal of Ginseng Research
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• v.16 no.3
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• pp.175-182
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• 1992

Intravenous administration of saponin from the root of Panax ginseng (red ginseng) lowered the blood pressure in a dose-dependent manner (10~100 mg/kg B.W) in anesthetized rats. Therefore, experiments were designed to study whether this lowering of blood pressure is associated with the release of endothelium-derived relaxing factor. Rings of thoracic aorta with and without endothelium were suspended for the measurement of isometric tension in organ chamber. All experiments were performed in the presence of indomethacin (10-5 M). Ginseng saponin (10-5~3$\times$10-4 g/ml) relaxed contractions induced by phenylephrine (10-5 M) in the aorta with endothelium but not in that without endothelium. Treatment of aortic rings with NG_monomethyl-L-arginine (L-NMMA 10-4 M for 30 min), a competive inhibitor of nitric oxide synthase and methylene blue (M.B., 3$\times$10-7 M for 30 min), an inhibitor of soluble guanylate cyclase, diminished the relaxation induced by ginseng saponin. In thoracic aortic rings from rats treated with ginseng saponin for 2 weeks intraperitoneally, the relaxation to acetylcholine was increased compared with non-ginseng treated rings. These data suggest that red ginseng saponin evokes hypotension and that vascular relaxations induced by red ginseng saponin are inediatpd by release of endothelium-derived relaxing factor.

• Journal of Cadastre & Land InformatiX
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• v.44 no.1
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• pp.195-212
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• 2014

This study was performed in order to contributing the influence factors in the real estate marketing strategy which largely affects the success of a real estate sale and development projects. Articles have to be concluded with the Influence factors of Satisfaction based on the type of Real Estate through PLS Regression Analysis. Building data was conducted by the target population specializing in the real estate sale and development business. Classification of real estate business classified by the way of the residential and non-residential parted. In the case of Housing type in the analysis result, the main factors were made by calculating the each factor such as brand trust, Strengthening the alliance and partnership, Traffic environment, Relaxing the requirements for a Real estate sales, Business presentation, Unsold benefits and Relaxing the requirements for payment. Otherwise, In the case of non-residential in the analysis result, the factors such as Relaxing the requirements for payment, Customer Orientation, living environment, Unsold benefits, Strengthening the alliance and partnership and communication terms made an influence to satisfaction.