• The Journal of Korean Medicine
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• v.24 no.1
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• pp.141-154
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• 2003

Objectives : This study was undertaken to define the effect of Diospyros kaki L. Radix or Diospyros kaki L. Folium on phenylephrine-induced arterial contraction and the mechanism of Diospyros kaki L. Radix or Diospyros kaki L. Foliuminduced relaxation. Methods : In order to investigate the effect of Diospyros kaki L. Radix or Diospyros kaki L. Folium on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. Diospyros kaki L. Radix or Diospyros kaki L. Folium extract was infused into contracted arterial strips induced by phenylephrine. To analyze the mechanism of Diospyros kaki L. Radix or Diospyros kaki L. Folium-induced relaxation, Diospyros kaki L. Radix or Diospyros kaki L. Folium extract was infused into contracted arterial strips induced by phenylephrine after treatment with indomethacin, $N{\omega}-nitro-L-arginine$, methylene blue or tetraethylammonium chloride, and $Ca^{2+}$ was infused into contracted arterial strips induced by phenylephrine after treatment of Diospyros kaki L. Radix or Diospyros kaki L. Folium in a $Ca^{2+}$-free solution. Results : Diospyros kaki L. Radix or Diospyros kaki L. Folium showed relaxation effect on arterial strip with endothelium contracted by phenylephrine, but in the strips without endothelium, Diospyros kaki L. Radix or Diospyros kaki L. Folium-induced relaxation was significantly inhibited. The endothelium-dependent relaxation induced by Diospyros kaki L. Radix or Diospyros kaki L. Folium was decreased by pretreatment with $N{\omega}-nitro-L-arginine$ or methylene blue but it was not observed in the strips pretreated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied to the strips which were contracted by phenylephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. However, pretreatment with Diospyros kaki L. Radix or Diospyros kaki L. Folium inhibited contractile response to $Ca^{2+}$. Conclusions : Diospyros kaki L. Radix or Diospyros kaki L. Folium may suppress influx of extra- cellular $Ca^{2+}$ through the formation of nitric oxide in the vascular endothelial cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.6
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• pp.730-737
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• 2013

The purpose of this study is to investigate vasorelaxant effect of Epimedium koreanum(EK) extract on rabbit carotid artery. In this study, to determine vasorelaxant effect of EK extract on rabbit carotid artery, arterial rings with intact or damaged endothelium were used for experiment using organ bath, and were contracted by norepinephrine(NE). After being contracted, arterial rings were treated with EK extract in a dose-dependent manner To study its mechanism, the contracted arterial rings induced by NE were pretreated with indomethacin(IM), $N_{\omega}$-nitro-L-arginine(L-NNA), methylene blue(MB) or tetraethylammonium chloride(TEA) and 0.1 $mg/m{\ell}$ EK extract was added. To analyze the effect of the EK extract on influx of extracellular calcium chloride($Ca^{2+}$) in rabbit carotid artery, in $Ca^{2+}$-free krebs solution, krebs solution containing 1 mM $Ca^{2+}$ was infused into the contracted arterial ring by NE after pretreatment of EK extract. To measure the cytotoxicity of the EK extract, cell viability of human umbilical vein endothelial cell(HUVEC) was measured by MTT assay, and nitric oxide(NO) was measured by Griess reagent. The EK extract significantly was relaxed the arterial ring with intact endothelium contracted by NE, but the vasorelaxant effect of the EK extract was inhibited in the arterial rings with damaged endothelium. The vasorelaxant effect of the EK extract was not different between the IM-pretreatedand and non-treated arterial rings. The vasorelaxant effect of EK extract were significantly inhibited, when arterial rings were pretreated with L-NNA, TEA, MB. And in $Ca^{2+}$-free krebs solution, increasing of arterial contraction by $Ca^{2+}$ addition were also inhibited by the treatment of EK, but not significant. The treatment of EK extract was increased NO concentration in HUVEC. This study suggested that the vasorelaxant effect of EK extract would be related with EDHF and NO production and increasing of cyclic GMP.

• Journal of Physiology & Pathology in Korean Medicine
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• v.30 no.2
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• pp.101-108
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• 2016

This study is conducted to investigate vasorelaxant effect of Corni Fructus(CF) on rabbit carotid artery. To determine vasorelaxant effect of CF on rabbit carotid artery, arterial sections with intact or removed endothelium were used in this organ bath study. After being contracted by phenylephrine(PE), arterial sections were treated with CF extract in a dose-dependent manner. To identity its mechanism, the contracted arterial sections by PE were pretreated with indomethacin(IM), tetraethylammonium chloride(TEA), Nω-nitro-L-arginine(L-NNA) or methylene blue(MB) and 1.0 ㎎/㎖ CF extract. We also studied to confirm the effect on influx of extracellular calcium chloride(Ca²⁺) of the CF extract in rabbit carotid artery. To measure the cytotoxicity of the CF extract, cell viability of human umbilical vein endothelial cell(HUVEC) was measured by MTT assay. Generation of nitric oxide(NO) was also measured by Griess reagent. The arterial sections with intact endothelium were relaxed significantly by CF extract, but this effect was inhibited in the arterial sections with damaged endothelium. The vasorelaxant effect was inhibited significantly when arterial sections were pretreated with IM, TEA, L-NNA, MB. In Ca²⁺-free krebs solution, increasing of arterial contraction by Ca²⁺ was also inhibited by CF significantly. The treatment of CF extract increased NO concentration in HUVEC. This study suggested that the vasorelaxant effect of CF extract would be related with endothelium derived relaxing factor(EDRF) such as NO, prostacyclin(PGI₂), endothelium derived hyperpolarization factor(EDHF).

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.6
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• pp.1622-1628
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• 2005

This study was undertaken to define the effect of SoPung-Tang extract on hypertension in spontaneous hypertensive rat and norepinephrine- induced arterial contraction in rabbit. In order to investigate the effect of SoPung-Tang extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of SoPung-Tang extract-induced relaxation, SoPung-Tang extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, Nu-nitro-L-arginine, methylene blue or tetraethylammonium chloride. Blood pressure was significantly decreased five days after administration of SoPung-Tang extract. SoPung-Tang extract relax arterial strip with endothelium contracted by norepinephrine, but in the strips without endothelium, SoPung-Tang extract- induced relaxation was significantly inhibited. SoPung-Tang relax arterial strip contracted by norepinephrine, but in the strips contracted by high $K^+$, SoPung-Tang extract-induced relaxation was significantly inhibited. The endothelium-dependent relaxation induced by SoPung-Tang extract was decreased by the pre-treatment of $N{\omega}$-nitro-L-arginine or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of SoPung-Tang extract inhibited contractile response to $Ca^{2+}$. We suggest that SoPung-Tang could be applied effectively for hypertension and may suppress influx of extra-cellular $Ca^{2+}$ through the formation of nitric oxide in the vascular endothelial cells.

• Korean Journal of Oriental Medicine
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• v.11 no.1
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• pp.97-107
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• 2005

Objectives : This experiments were performed to determine the effect of Linderae Radix extract on norepinephrine-induced arterial contraction in rabbit. Methods : In order to investigate the effect of Linderae Radix extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of Linderae Radix extract-induced relaxation, Linderae Radix extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, tetraethylammonium chloride, $N{\omega}-nitro-L-arginine$ or methylene blue. Results : Linderae Radix extract relax arterial strip with endothelium contracted by norepinephrine, but in the strips without endothelium, Linderae Radix extract-induced relaxation was significantly inhibited. Linderae Radix extract-induced relaxation was decreased by the pre-treatment of $N{\omega}-nitro-L-arginine$ or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of Linderae Radix extract inhibited contractile response to norepinephrine and $Ca^{2+}$. Conclusions : We suggest that Linderae Radix may suppress influx of extra-cellular $Ca^{2+}$ through the formation of nitric oxide, and release of intra-cellular $Ca^{2+}$.

• Korean Journal of Oriental Medicine
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• v.10 no.2
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• pp.79-92
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• 2004

Objectives : This experiments were performed to determine the effect of OYakSoonGi-San extract on hypertension in spontaneous hypertensive rat and norepinephrine-induced arterial contraction in rabbit. Methods : In order to define the effect of OYakSoonGi-San extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of OYakSoonGi-San extract-induced relaxation, OYakSoonGi-San extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, $N{\omega}-nitro-L-arginine$, methylene blue or tetraethylammonium chloride. Results : Blood pressure was significantly decreased five days after administration of OYakSoonGi-San extract. The relaxation effect of OYakSoonGi-San extract was dependent on the presence of endothelium, showing that OYakSoonGi-San extract-induced relaxation was not observed in the strips without endothelium. Also OYakSoonGi-San extract-induced relaxation was significantly inhibited in arterial strips which were contracted by high $K^+$. OYakSoonGi-San extract-indeced relaxation was significantly inhibited by the pre-treatment of $N{\omega}-nitro-L-arginine$ or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When additive application of $Ca^{2+}$ in arterial strips which were pre-contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But contractile response to $Ca^{2+}$ was attenuated by pre-treatment of OYakSoonGi-San extract. Conclusions : These results demonstrated that OYakSoonGi-San could be applied effectively to hypertension and may inhibit agonist-induced contraction through an decrease influx of extra-cellular $Ca^{2+}$ by the formation of nitric oxide in the vascular endothelial cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.1
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• pp.112-117
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• 2013

We studied the modulation of pacemaker activities by Samchulkunbi-tang (SCKB) in cultured interstitial cells of Cajal (ICC) from murine small intestine with the whole-cell patch-clamp technique. Externally applied SCKB produced membrane depolarization in the current-clamp mode. The pretreatment with $Ca^{2+}$-free solution and thapsigargin, a $Ca^{2+}$-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker potentials and suppressed the SCKB-induced action. The application of flufenamic acid (a nonselective cation channel blocker) abolished the generation of pacemaker potentials by SCKB. However, the application of niflumic acid (a chloride channel blocker) did not inhibit the generation of pacemaker potentials by SCKB. In addition, the membrane depolarizations were inhibited by not only GDP-${\beta}$-S, which permanently binds G-binding proteins, but also U-73122, an active phospholipase C inhibitor. These results suggest that SCKB modulates the pacemaker activities by nonselective cation channels and external $Ca^{2+}$ influx and internal $Ca^{2+}$ release via G-protein and phospholipase C-dependent mechanism. Therefore, the ICC are targets for SCKB and their interaction can affect intestinal motility.

• Journal of Physiology & Pathology in Korean Medicine
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• v.27 no.5
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• pp.563-569
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• 2013

This study was undertaken to apply the yin-yang theory in action potential. In order to apply the yin-yang theory in action potential, nature of yin and yang, interrelation of yin and yang and action potential in cell were reviewed. According to the yin-yang theory, inner cellular space corresponds to yin, but outer cellular space corresponds to yang. If we classify ions in intracellular fluid or extracellular fluid by nature of yin and yang, potassium(K+) corresponds to yang within yin(陰中之陽), protein(Pr-) corresponds to yin within yin(陰中之陰) in intracellular fluid, and sodium(Na+) corresponds to yang within yang(陽中之陽), chloride(Cl-) corresponds to yin within yang(陽中之陰) in extracellular fluid. Double donnan equilibrium and equilibrium potential were caused by intracellular anion(Pr-) and extracellular cation(Na+) are related with mutual rooting of yin and yang(陰陽互根) and opposition of yin and yang(陰陽對立). The influx and efflux of ion through cell membrane means waxing and waning of yin and yang(陰陽消長), the change of membrane potential means yin-yang conversion(陰陽轉化) during action potential.

• Natural Product Sciences
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• v.22 no.4
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• pp.263-269
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• 2016

Rhynchophylline (RP) is a major tetracyclic oxindole alkaloid of Uncariae Ramulus et Uncus which has been used to treat hypertension, seizures, pain and anxiety in the oriental countries. A recent report revealed that RP attenuated ischemia-induced neuronal damage and kainite-induced convulsions in animals. This study was performed to investigate whether RP enhances pentobarbital-induced sleep behaviors and modulates sleep architecture in mice. Locomotor activity was significantly inhibited by RP at 0.25 and 0.5 mg/kg, similar to 2 mg/kg diazepam (a benzodiazepine agonist) in mice. RP shortened sleep latency and increased total sleep time in a dose-dependent manner when administrated with pentobarbital (42 mg/kg, i.p.). RP also increased the number of sleeping mice and total sleep time by concomitant administration with the sub-hypnotic dosage of pentobarbital (28 mg/kg, i.p.). On the other hand, RP (0.25 mg/kg, p.o.) itself significantly inhibited sleep-wake cycles, prolonged total sleep time, and rapid eye movement in rats. In addition, RP also increased chloride influx in the primary cultured hypothalamic neuronal cells. In addition, we found that glutamic acid decarboxylase ($GAD_{65/67}$) was activated by RP. In conclusion, RP augments pentobarbital-induced sleeping behaviors, and can be a candidate for treating insomnia.

• 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.