• Title/Summary/Keyword: 1,3,4 oxadiazole

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Effect of Acorus Gramineus on the Relaxation of Corpus Cavernosum Smooth Muscle (석창포에 의한 발기부전 개선 효과)

  • Li, Xiang;Kim, Ho-Tae;Lee, Jae-Yun;Lee, Yun-Jung;Shin, Hong-Kyun;Kang, Dae-Gill;Lee, Ho-Sub
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.25 no.5
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    • pp.863-869
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    • 2011
  • The aim of the present study is to investigate whether an ethanol extract of Acorus gramineus Soland (EAG) augments penile erection in vitro and in vivo experiment. Preconstructed with phenylephrine (PE) in isolated endothelium-intact rabbit corpus cavernosum, EAG relaxed penile smooth muscle in a dose-dependent manner, which was inhibited by pretreatment with NG-nitro-L-argininemethylester (L-NAME), a nitricoxide synthase inhibitor, and 1H-[1,2,4]-oxadiazole-[4,3-${\alpha}$]-quinoxalin-1-one (ODQ), a soluble guanylylcyclase (sGC) inhibitor, respectively. EAG-induced relaxation was significantly attenuated by pretreatment with tetraethylammonium (TEA), a nonselective $K^+$ channel blocker. EAG increased cGMP levels of the rabbit corpus cavernosum in a concentration-dependent manner without changes in cAMP levels. In addition, EAG caused increase of peak intracavernous pressure (ICP), ICP/MAP ratio and area under the carve (AUC) in SD rats. Taken together, these results suggest that EAG augments penile erection via NO-cGMP system and $K^+$ channels in corpus cavernosum.

Mechanism for the Vascular Relaxation Induced by Butanol Extract of Agrimonia pilosa (선학초 부탄올 추출물의 혈관 이완 효과의 기전에 대한 연구)

  • Hua, Cao-Li;Lee, Jun-Kyung;Cho, Kuk-Hyun;Kwon, Tae-Oh;Kwon, Ji-Woong;Kim, Jin-Sook;Sohn, Eun-Jin;Lee, Ho-Sub;Kang, Dae-Gill
    • Korean Journal of Pharmacognosy
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    • v.37 no.2 s.145
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    • pp.67-73
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    • 2006
  • The butanol extracts of Agrimonia pilosa (BAP) induced dose-dependent vascular 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 methyl ester (L-NAME) and 1H-[1,2,4]-oxadiazole-[$4,3-{\alpha}$]-quinoxalin-1-one(ODQ) inhibited the relaxation induced by BAP. BAP-induced vascular relaxation was also markedly attenuated by addition of verapamiI, while the relaxant effect of BAP was not blocked by indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, or propranolo. In addition, incubation of endothelium-intact aortic rings with BAP increased the vascular production of cGMP. These results suggest that BAP relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling pathway, which may be causally related with L-type $Ca^{2+}$ channels.

Effect of Lophatherum gracile on the mechanism of vasorelaxation in thoracic aorta (담죽엽 추출물의 혈관이완 기전에 대한 연구)

  • Kim, Hye-Yoom;Li, Xiang;Lee, Yun-Jeong;Seo, Hwan-Ho;Cho, Nam-Geun;Kang, Dae-Gill;Lee, Ho-Sub
    • Herbal Formula Science
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    • v.17 no.2
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    • pp.175-186
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    • 2009
  • The vasorelaxant effect of an extract of Lophatherum gracile Brongn (ELB) and its possible action mechanism were ascertained in aortic tissues isolated from rats. ELB relaxed endothelium-intact thoracic aorta in a dose-dependent manner. However, the induced vascular relaxation was abolished by removal in endothelium of the thoracic aorta. Pretreatment of endothelium-intact vascular tissues with $N^G$-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-$\alpha$]-quinoxalin-1-one (ODQ) significantly inhibited vascular relaxation induced by ELB. Moreover, ELB significantly increased cGMP production in aortic tissues, which was blocked by pretreatment with L-NAME or ODQ. The vasorelaxant effect of ELB was attenuated by tetraethylammonium (TEA), and glibenclamide. ELB-induced vasorelaxation was not blocked by atropine, propranolol, indomethacin, verapamil, and diltiazem. Taken together, the present study demonstrates that ELB dilates vascular smooth muscle via an endothelium-dependent NO-cGMP signaling pathway, which may be at least in part related with the function of $K^+$ channels.

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Study on the Mechanism of Vascular Relaxation Induced by Cortex Caryphylli (정향피 추출물의 혈관 이완효과 및 작용기전에 대한 연구)

  • Song, Chul-Min;Shin, Sun-Ho;Jung, Hyun-Ae;Lee, Jun-Kyoung;Cao, Li-Hua;Kang, Dae-Gil;Lee, Ho-Sup
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.5
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    • pp.1166-1173
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    • 2006
  • The aqueous extracts of Cortex Caryophylli (AEC) 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 methyl ester (L-NAME) or 1 H-[1,2,4]-oxadiazole-[4,3-${\alpha}$l-quinoxalin-1-one (ODQ) inhibited the relaxation induced by AEC. AEC-induced vascular relaxations were also markedly attenuated by addition of verapamil, diltiazem and glibenclamide, tetraethylammonium (TEA), respectively, while the relaxation effect of AEC was not blocked by indomethacin, atropine, or propranolol. Moreover, incubation of endothelium-intact aortic rings with AEC increased the production of cGMP. These results suggest that AEC dilates vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling, which seems to be causally related with L-type Ca$^{2+}$ and K$^+$ channels.

Vascular Relaxation Induced by the Water Soluble Fraction of the Seeds from Oenothera Odorata (월견자 물 분획층을 이용한 혈관이완 기전에 관한 연구)

  • Kim, Hye Yoom;Lee, Yun Jung;Yoon, Jung Joo;Kho, Min Chol;Han, Byung Hyuk;Choi, Eun Sik;Park, Ji Hun;Kang, Dae Gill;Lee, Ho Sub
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.29 no.6
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    • pp.492-497
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    • 2015
  • In the present study, vasorelaxant effect of the extract of seeds of Oenothera odorata (SOO) and its possible mechanism responsible for this effect were examined in vascular tissues isolated from rats. Changes in vascular tension, 3',5'-cyclic monophosphate (cGMP) levels were measured in thoracic aorta rings from rats. Methanol extract of seeds of Oenothera odorata relaxed endothelium-intact thoracic aorta in a dose-dependent manner. A dose-dependent vascular relaxation was also revealed by treatment of ethylacetate, n-butanol, and H2O (aqua extract of seeds of Oenothera odorata , ASOO) extracts partitioned from methanol, but not by hexane extract. However, the vascular relaxation induced by ASOO were abolished by removal of endothelium of aortic tissues. Pretreatment of the endothelium-intact vascular tissues with NG-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-α]-quinoxalin-1- one (ODQ) significantly inhibited vascular relaxation induced by ASOO. Moreover, incubation of endothelium-intact aortic rings with ASOO increased the production of cGMP. However, ASOO-induced increases in cGMP production were blocked by pretreatment with L-NAME or ODQ. The vasorelaxant effect of ASOO was attenuated by tetraethylammonium (TEA), 4-aminopyridine, and glibenclamide attenuated. On the other hand, the ASOO-induced vasorelaxation was not blocked by verapamil, and diltiazem. Taken together, the present study demonstrates that ASOO dilate vascular smooth muscle via endothelium-dependent NO-cGMP signaling pathway, which may be closely related with the function of K+ channels.

Effect of Mixed Herbicides on Phytotoxicity of Azimsulfuron in Rice and Barnyardgrass (벼와 피에 대한 Azimsulfuron의 작용성(作用性)에 미치는 혼합제초제(混合除草劑)의 영향(影響))

  • Chun, J.C.;Ma, S.Y.;Kim, S.E.
    • Korean Journal of Weed Science
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    • v.15 no.3
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    • pp.232-237
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    • 1995
  • Effect of azimsulfuron {1-(4,6-dimethoxypyrimidin-2-yl)-3-[1-methyl-4-(2-methyl-2H-tetrazol-5-yl) pyrazol-5-ylsulfonl]urea} combined with eight annual herbicides on shoot and root growth of rice (Oryza sativa L.) and barnyardgrass [Echinochloa crus-galli (L.) P. Beauv.] was investigated. Annual herbicides used were four thiocarbamates (dimepiperate, molinate, esprocarb, and thiobencarb), two acetanilides (butachlor and pretilachlor), one urea (dymron), and one oxadiazole (oxadiazon) herbicide. Growth inhibition in rice shoot was greater with azimsulfuron mixed with the annual herbicides than with azimsulfuron only. The azimsulfuron mixtures did not bring about decrease in growth inhibition of rice shoot. However, safening effect in root growth of rice was obtained when dimepiperate, molinate and dymron were combined with greater than 10ppm of azimsulfuron. Greater inhibition in shoot and root growth of rice occurred with straight chain hydrocarbon substitute such as esprocarb and thiobencarb than with cyclohydrocarbon substitute such as dimepiperate and molinate. Application of the azimsulfuron mixtures resulted in increase. in growth inhibition of shoot and root growth of barnyardgrass as compared with when azimsulfuron only was applied.

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Study on the Mechanism of Vascular Relaxation of Methanol Extract of Rose multiflora Radix (장미근(薔薇根) 메탄올 추출물의 혈관이완 기전에 대한 연구)

  • Kim, Dae-Joong;Jo, Nam-Geun;Lee, Jun-Kyoung;Cao, Li-Hua;Lee, Hyuck;An, Jung-Seok;Um, Jae-Yeon;Joe, Gye-One;Na, Han-Il;Kyung, Eun-Ho;Kang, Dae-Gil;Lee, Ho-Sub
    • 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.