• 제목/요약/키워드: L-NAME

검색결과 450건 처리시간 0.029초

한국 미기록 귀화식물: 가는끈끈이장구채(석죽과) (Newly Recorded Naturalized Species in Korea, Silene antirrhina L. (Caryophyllaceae))

  • 박규진;고재기;박재홍
    • 식물분류학회지
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    • 제41권2호
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    • pp.171-174
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    • 2011
  • 대구광역시에 위치한 금호강 강변에서 발견된 석죽과의 Silene antirrhina L.를 한반도 미기록종으로 확인하여 보고한다. 본 종은 속 내의 근연종인 끈끈이장구채(S. koreana Kom.) 및 끈끈이대나물(S. armeria L.)과 같이 선점이 있으나 개화시 수술이 꽃받침 밖으로 외출하지 않고, 종자의 표면이 유두상 돌기인 점에서 근연종과 뚜렷이 구분된다. 국명은 식물체가 소형이고 전체적으로 가는 점을 고려하여 '가는끈끈이장구채'로 명명하였으며, 생태사진과 주요 형질에 대한 기재 및 검색표를 제시하였다.

Mechanism of L-NAME-Resistant Endothelium-Dependent Relaxation Induced by Acetylcholine in Rabbit Renal Artery

  • Yeon, Dong-Soo;Ahn, Duck-Sun;Lee, Young-Ho;Kwon, Seong-Chun
    • The Korean Journal of Physiology and Pharmacology
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    • 제4권6호
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    • pp.471-477
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    • 2000
  • In the rabbit renal artery, acetylcholine $(ACh,\;1\;nM{\sim}10\;{\mu}M)$ induced endothelium-dependent relaxation of arterial rings precontracted with norepinephrine $(NE,\;1\;{\mu}M)$ in a dose-dependent manner. $N^G-nitro- L-arginine$ (L-NAME, 0.1 mM), an inhibitor of NO synthase, or ODQ $(1\;{\mu}M),$ a soluble guanylate cyclase inhibitor, partially inhibited the ACh-induced endothelium-dependent relaxation. The ACh-induced relaxation was abolished in the presence of 25 mM KCl and L-NAME. The cytochrome P450 inhibitors, 7- ethoxyresorufin $(7-ER,\;10\;{\mu}M),$ miconazole $(10\;{\mu}M),$ or 17-octadecynoic acid $(17-ODYA,\;10\;{\mu}M),$ failed to inhibit the ACh-induced relaxation in the presence of L-NAME. 11,12-epoxyeicosatrienoic acid $(11,12-EET,\;10\;{\mu}M)$ had no relaxant effect. The ACh-induced relaxation observed in the presence of L-NAME was significantly reduced by a combination of iberiotoxin $(0.3\;{\mu}M)$ and apamin $(1\;{\mu}M),$ and almost completely blocked by 4-aminopyridine (5 mM). The ACh-induced relaxation was antagonized by $P_{2Y}$ receptor antagonist, cibacron blue $(10\;and\;100\;{\mu}M),$ in a dose-dependent manner. Furthermore, 2-methylthio-ATP (2MeSATP), a potent $P_{2Y}$ agonist, induced the endothelium-dependent relaxation, and this relaxation was markedly reduced by either the combination of iberiotoxin and apamin or by cibacron blue. In conclusion, in renal arteries isolated from rabbit, ACh produced non-NO relaxation that is mediated by an EDHF. The results also suggest that ACh may activate the release of ATP from endothelial cells, which in turn activates $P_{2Y}$ receptor on the endothelial cells. Activation of endothelial $P_{2Y}$ receptors induces a release of EDHF resulting in a vasorelaxation via a mechanism that involves activation of both the voltage-gated $K^+$ channels and the $Ca^{2+}-activated\;K^+\;channels$. The results further suggest that EDHF does not appear to be a cytochrome P450 metabolite.

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해바라기(향일규(向日葵), 향일화(向日花))의 어원(語源)에 대하여 (The origin of the word of sunflower)

  • 김종덕;고명희
    • 한국한의학연구원논문집
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    • 제7권1호
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    • pp.55-66
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    • 2001
  • According to the customary, naming is done after the subject is in existence. But the name's Hae-ba-ra-gi(해바라기), 향일규(向日葵), 향일화(向日花))' has been used as an alias of Hibiscus manihot L.(닥풀) long before Helianthus annuus L.(sunflower) was brought in to Korea. And now the usage of the name has been conversed since them. Since the incorrect record of '葵藿' and '葵花'as '해바라기' in ${\ulcorner}$조선어사전(朝鮮語辭典)${\lrcorner}$(1920), the mistake has been carried on this must be corrected from now on. Incorrect record of hollyhock(蜀葵花) '해바라기' in ${\ulcorner}$몽유(蒙喩))${\lrcorner}$(1810) took a role in this incorrect trend.

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Interaction of Nitric Oxide and Renin Angiotensin System in Pulmonary Arterial Circulation of RHR

  • Lee, Byung-Ho;Shin, Hwa-Sup
    • Archives of Pharmacal Research
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    • 제20권5호
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    • pp.389-395
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    • 1997
  • We investigated the interaction between nitric oxide and the renin angiotensin system in regulating isolated pulmonary arterial tension and pulmonary arterial pressure (PAP) in renal hypertensive rats (RHR) made by complete ligation of left renal artery. Losartan induced a depressor response that was smaller in RHR than in normotensive rats (NR) (3.3 and 7.0 mmHg, respectively, at 3.0 mg/kg, p<0.05), and the response was significantly reduced by $N^{G}$-nitro-Larginine methyl ester (L-NAME). Angiotensin II elevated the PAP (7.6 and 10.8 mmHg at $0.1 {\mu}g/kg$; 20.3 and 23.6 mmHg at $1.0{\mu}g/kg$, respectively) and contracted the isolated pulmonary artery ($pD_2$: 8.79 and 8.71, respectively) from both NR and RHR with similar magnitude, and these effects were significantly enhanced by L-NAME in NR, but not in RHR. Acetylcholine lowered the PAP slightly less effectively in RHR than in NR (3.8 and 6.0 mmHg at 10 .mu.g/kg, respectively) and relaxed the pulmonary artery precontracted with norepinephrine in both rats with similar magnitude ($E_max$: 60.8 and 63.6%, respectively), and the effect being completely abolished after pretreatment.with L-NAME or removal of endothelial cells. These results suggest that nitric oxide interacts with renin angiotensin system to control the pulmonary vascular tension and pulmonary arterial circulation of RHR.R.

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SKF 525A가 휜쥐의 대동맥에서 Sodium nitroprusside, Acetylcholine, Pinacidil에 의한 이완반응에 미치는 효과 (The effect of SKF S25A on SNP-, Ach-, or Pinacidil-Induced Relaxation in the Aorta of Rat)

  • 박조영;김학림;김주원;신창열;최윤미;김진학;안형수;손의동;허인회
    • 약학회지
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    • 제44권1호
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    • pp.80-86
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    • 2000
  • TEA, glibenclamide, L-NAME and SKF 525A-induced contraction were investigated using acetylcholine, sodium nitroprusside (SNP, NO donor) and pinacidil (ATP sensitive $K^{+}$ channel opener) in rat abdominal and thoracic aorta. The relaxant effects of acetylcholine, SNP and pinacidil were not different in the abdominal aorta and in the thoracic aorta. Acetylcholine-induced relaxation was dependent on endothelial cell, but pinacidil was independent endothelia cell. In the presence of TEA, glibenclamide, L-NAME, mepacrine and SKF 525A, acetylcholine and SNP did not change, but pinacidil-induced relaxation was significantly reduced in presence of glibenclamide, which is ATP sensitive $K^{+}$ channel blocker. SKF 525A, which is inhibitor of cytochrome P$_{450}$ dependent epoxygenase, partially inhibited the pinacidil-induced relaxation. These results indicate that the pinacidil-induced relaxation may be mediated by ATP sensitive $K^{+}$ channel and partially by EETs, which is produced by cytochrome P$_{450}$ dependent epoxygenase.enase.

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Effect of age on endothelial function in rat aorta

  • 정이숙;조태순;신화섭
    • 한국응용약물학회:학술대회논문집
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    • 한국응용약물학회 1995년도 춘계학술대회
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    • pp.90-90
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    • 1995
  • The Influence of age on the endothelial modulation of angiotensin II (AII)-induced contractile response was investigated in isolated aortic rings of rats ranging in age from 0.7 to 20 months. Hemoglobin and L-NAME were used to examine whether age-related changes in the EDRF-releasing system were involved in endothelial modulation of All-induced contraction in rat aorta. In all five age groups (0.7, 1.5, 3, 6, 20 months), hemoglobin (10 ${\mu}$M) significantly enhanced All-induced contractile response only in aorta with endothelium intact. L-NAME (10 ${\mu}$M) Produced a significant enhancement in All responses in endothelium-intact aortas from rats aged 0.7 and 1.5 months, but it had no effect in aortas from older rats aged 6 and 20 months. Indomethacin (10 ${\mu}$M) did not affect All-induced contractile responses in both endothelium intact and removed aortas from rats at the age of 0.7 to 20 months. Hemoglobin (10 ${\mu}$M) abolished acetylcholine-induced relaxation response in aortas from young and old rats. L-NAME completely abolished the relaxation in aortas from young (0.7 and 1.5 months), but incompletely in aortas from older (6 and 20 months) rats. The sensitivity of endothelium-dependent relaxation to A23187 increased with age between ages of 0.7 and 6 months, with no further increase noted up to 20 months of age. These results suggest that endothelial modulation of AII-induced contraction in rat aorta might involve age-related alteration in EDRF-releasing system, probably via post-receptor mechanism.

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NOS만성억제로 인한 고혈압에서 아드레날린성 활성증가기전 (Mechanism of Increased Adrenergic Activities in Hypertension Induced by Chronic Inhibition of NOS)

  • 정국현;이석용
    • 약학회지
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    • 제45권1호
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    • pp.85-92
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    • 2001
  • Nitric oxide is a tonically produced vasodilator that maintains blood pressure in the normal animal. The chronic inhibition of nitric oxide synthase (NOS) elicits the hypertension in rats. However, the mechanism of hypertension induced by chronic inhibition of NOS is not clear. Thus, to clarify the mechanism of the occurance of hypertension, the changes in $\alpha$-adrenergic systems in rats treated with NOS inhibitors for 21 days were examined. Chronic administration of L-NAME significantly increased in the basal blood pressure, but chronic administration of 7-nitroindazole did not. Phenylephrine and G-protein stimulator elicited the more potent contraction in the aorta of the L-NAME-induced hypertensive rats. However when the contractile responses by phenylephrine and G-protein stimulator were calculated the proportion to the contraction by 25 mM KCL, there was no difference between the vehicle-treated rats and the L-NAME-treated rats. The density of $\alpha$-adrenergic receptors in aortic tissue was not changed by the chronic inhibition of NOS. These results suggest that hypertension induced by chronic inhibition of NOS is due to the inhibition of eNOS and the increased responses to the adrenergic drugs are due to the changes of the intracellular contactile mechanism of aortic tissue rather than the changes of receptor density.

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세균 내독소 유발 혈관 저반응성에 대한 $N^G$-nitro-L-arginine methyl ester와 Methylene blue의 영향 (Effect of $N^G$-nitro-L-arginine methyl ester and Methylene Blue on the Endotoxin-induced Vascular Hyporesponsiveness)

  • 최형철;하정희;이광윤;김원준;손의동
    • Journal of Yeungnam Medical Science
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    • 제14권2호
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    • pp.337-349
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    • 1997
  • 세균 내독소에 의하여 발생하는 패혈성 쇼크와 혈관 반응성 감소의 원인을 관찰하였다. 혈관 절편이 고정된 실험조에 세균 내독소 0.2 mg 투여한 경우 $36{\pm}3.65$ nM NO가 발생되었고, NO 발생에 의한 혈관 이완 효과를 억제하기 위해 전처치한 L-MAME, methylene blue는 혈관 절편의 phenylephrine (PE) 유발 수축 반응을 증가시켰으며 methylene blue에 의해 더 강한 수축 반응의 증가가 관찰되었다. 이때 혈관 내피세포가 존재할 경우에 PE에 대한 혈관 반응성이 증가되는 경향을 나타내었다. 세균 내독소 투여에 의해 acetylcholine 유발 혈관 이완은 증가되는 경향을 나타내었고, 전처치한 L-NAME, methylene blue에 의해 혈관 절편의 acetylcholine (ACh) 유발 이완은 억제되었으며 methylene blue에 의해 현저히 억제되었다. 그러나 세균 내독소를 투여하지 않은 군의 ACh 유발 혈관 이완 반응은 methylene blue에 의해서만 억제되었다. 결론적으로 세균 내독소에 의한 혈관 반응성 감소와 혈관 이완 반응은 NO가 발생되어 guanylyl cyclase를 활성화하여 유발된다고 생각되며, 세균 내독소에 의한 효과는 L-arginine NO pathway 보다는 cyclic GMP 신호전달계를 경유한 경로에서 더 많은 영향을 받는것으로 사료된다.

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신경병성 통증모델쥐에서 산화질소합성효소 억제제가 척수후각세포의 활성도에 미치는 영향 (Effects of NO Synthase Inhibitor on Responsiveness of Dorsal Horn Neurons in Neuropathic Pain Animal Model)

  • 임중우;곽영섭;정승수;이규래;윤덕미;남택상
    • The Korean Journal of Pain
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    • 제13권1호
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    • pp.19-30
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    • 2000
  • Background: Partial nerve injury to a peripheral nerve may induce the development of neuropathic pain which is characterized by symptoms such as spontaneous burning pain, allodynia and hyperalgesia. Though underlying mechanism has not fully understood, sensitization of dorsal horn neurons may contribute to generate such symptoms. Nitric oxide acts as an inter- and intracellular messenger in the nervous system and is produced from L-arginine by nitric oxide synthase (NOS). Evidence is accumulating which indicate that nitric oxide may mediate nociceptive information transmission. Recently, it has been reported that NOS inhibitor suppresses neuropathic pain behavior in an neuropathic pain animal model. This study was conducted to determine whether nitric oxide could be involved in the sensitization of dorsal horn neurons in neuropathic animal model. Methods: Neuropathic animal model was made by tightly ligating the left L5 and L6 spinal nerves and we examined the effects of iontophoretically applied NOS inhibitor (L-NAME) on the dorsal horn neuron's responses to mechanical stimuli within the receptive fields. Results: In normal animals, NOS inhibitor (L-NAME) specifically suppressed the responses to the noxious mechanical stimuli. In neuropathic animals, the dorsal horn neuron's responses to mechanical stimuli were enhanced and NOS inhibitor suppressed the dorsal horn neuron's enhanced responses to non-noxious stimuli as well as those to noxious ones. Conclusions: These results suggest that nitric oxide may mediate nociceptive transmission in normal animal and also mediate sensitization of dorsal horn neurons in neuropathic pain state.

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수소음심경 오수혈 혈위별 레이저 침자가 고혈압 흰쥐의 혈압에 미치는 영향 (The Effect of Laser Acupuncture of Five-Transport-Points of the Heart Meridian in L-NAME-Induced Hypertensive Rats)

  • 신욱;이유미;김왕인;최동희;김미래;윤대환;나창수
    • Korean Journal of Acupuncture
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    • 제34권1호
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    • pp.56-69
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    • 2017
  • Objectives : The purpose of this study is to compare the effects of laser acupuncture to the 532 nm on the five transport points with the heart meridian for treatment to hypertensive disease in rats with L-NAME induced hypertensive. Methods : Hypertensive was induced by L-NAME for 3 weeks. The laser acupuncture therapy on the five transport points of heart meridian(Laser Well Point-HT9, Laser Brook Point-HT8. Laser Stream Point-HT7, Laser River Point-HT4 and Laser Sea Point-HT3) was treated twice a week for 5 times. The hypertensive was measured using a cardiac hypertrophy, atherogenic index, TG/HDL-cholesterol ratio, TCHO, HDLC, TG, AST, ALT, antioxidative effectiveness and glutathione peroxidase quality of hypertensive rats induced by L-NAME. Results : Blood pressure were decreased significantly after the laser acupuncture of Well, Brook and Sea Point groups. Cardiac hypertrophy were decreased at the laser acupuncture of Brook and Stream Point groups. Athrogenic index was decreased at the laser acupuncture of Well, Stream, River and Sea Point groups. TG/HDL-cholesterol ratio was decreased at the laser acupuncture of all groups. Total cholesterol was decreased significantly at the laser acupuncture of Well Point group. High density lipoprotein cholesterol and total cholesterol were decreased significantly at the laser acupuncture of Well, Stream and River Point groups. Triglyceride was decreased significantly at the laser acupuncture of Stream Point group. Cu/Zn-Superoxide Dismutase (Cu/Zn-SOD) and glutathione peroxidase(GPX) were increased significantly at the laser acupuncture of Well Point group. Conclusions : The laser acupuncture treatment in five transport points of the Heart Meridian was effective for lowering blood pressure, cardiac hypertrophy, Atherogenic index and HTR, and for enhancing antioxidant activity.