• Proceedings of the Korean Society of Life Science Conference
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• 2005.09a
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• pp.122-122
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• 2005

• Proceedings of the Korean Nutrition Society Conference
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• 1998.11a
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• pp.75-75
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• 1998

• Proceedings of the Zoological Society Korea Conference
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• 1995.10b
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• pp.264.2-264
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• 1995

No Abstract, See Full Text

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.485-493
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• 2005

We studied the effects of trazodone on arterial blood pressure in anesthesized guinea pigs, and on vascular responses in isolated thoracic aorta. Trazodone produced a concentration-dependent relaxation in phenylephrine-precontracted endothelium intact (+E) rings, but not in a KCl-precontracted aortic rings. These relaxant effects of trazodone on +E rings were significantly greater than those on denuded (-E) rings. The trazodone-induced relaxation was suppressed by glibenclamide and tetrabutylammonium, but not by N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), methylene blue (MB), nifedipine, indomethacin, 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC) and clotrimazole. In vivo, infusion of trazodone elicited a significant decrease in arterial blood pressure. Trazodone-induced blood pressure lowering was markedly inhibited by intravenous pretreatment of prazosin but not by pretreatment of saponin, L-NNA, L-NAME, MB, nifedipine, glibenclamide, clotrimazole and NCDC. In addition, trazodone produced an increase in twitch force of isolated papillary muscle and left ventricular pressure of perfused heart. These findings suggest that the endothelium-independent vasorelaxant effect of trazodone may be explained by activation of $Ca^{2+}$-activated and ATP-sensitive $K^+$ channels, and the hypotensive effect of trazodone is not associated with cardiac contraction.

• Journal of dental hygiene science
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• v.15 no.6
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• pp.800-806
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• 2015

The aim of this study was to investigate whether intracisternal administrations of triptolide and N-nitro-L-arginine Methyl Ester (L-NAME) are involved in the regulation of temporomandibular joint (TMJ) pain. The TMJ pain was induced by the injection of 5% formalin ($30{\mu}l$) into TMJ capsule of rats. The pain behavioral responses was recorded the number of grooming or scratching on the left TMJ area for 9 successive 5 minutes intervals. Triptolide and L-NAME were administrated intracisternally 10 minutes before formalin injection. The intra-articular injection of formalin produced a biphasic pattern of pain response (first phase: 0~10 minutes and second phase: 11~45 minutes). The intracisternal administration of triptolide ($1{\mu}g/10{\mu}l$) and L-NAME ($0.1{\mu}g/10{\mu}l$) suppressed the TMJ pain behavior in each experiment. Co-administration of two drugs was shown the enhanced effect than the analgesic effect by single-administration of triptolide ($1{\mu}g/10{\mu}l$). The triptolide could be a useful analgesic agent for the treatment of TMJ pain, and it is expected to reduce the substantial amount of it via co-administration of synthetic chemical compound and natural products.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.231-238
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• 1994

Backgroud: Since the demonstration of the fact that vascular relaxation by acetylcholine(Ach) results from the release of relaxing factor from the endothelium, the identity and physiology of this endothelium-derived relaxing factor(EDRF) has been the target for many researches. EDRF has been identified as nitric oxide(NO). With the recent evidences that EDRF is an important mediator of vascular tone, there have been increasing interests in defining the role of the EDRF as a potential mediator of hypoxic pulmonary vasoconstriction. But the role of EDRF in modulating the pulmonary circulation is not compeletely clarified. To investigate the endothelium-dependent pulmonary vasodilation and the role of EDRF during hypoxic pulmonary vasoconstriction, we studied the effects of $N^G$-monomethyl-L-arginine(L-NMMA) and L-arginine on the precontracted pulmonary arterial rings of the rat in normoxia and hypoxia. Mothods: The pulmonary arteries of male Sprague Dawley(300~350g) were dissected free of surrounding tissue, and cut into rings. Rings were mounted over fine rigid wires, in organ chambers filled with 20ml of Krebs solution bubbled with 95 percent oxygen and 5 percent carbon dioxide and maintained at $37^{\circ}C$. Changes in isometric tension were recorded with a force transducer(FT.03 Grass, Quincy, USA) Results: 1) Precontraction of rat pulmonry artery with intact endothelium by phenylephrine(PE, $10^{-6}M$) was relaxed completely by acetylcholine(Ach, $10^{-9}-10^{-5}M$) and sodium nitroprusside(SN, $10^{-9}-10^{-5}M$), but relaxing response by Ach in rat pulmonary artery with denuded endothelium was significantly decreased. 2) L-NMMA($10^{-4}M$) pretreatment inhibited Ach($10^{-9}-10^{-5}M$)-induced relaxation, but L-NMMA ($10^{-4}M$) had no effect on relaxation induced by SN($10^{-9}-10^{-5}M$). 3) Pretreatment of the L-arginine($10^{-4}M$) significantly reversed the inhibition of the Ach ($10^{-9}-10^{-5}M$)-induced relaxation caused by L-NMMA($10^{-4}M$) 4) Pulmonary arterial contraction by PE($10^{-6}M$) was stronger in hypoxia than normoxia but relaxing response by Ach($10^{-9}-10^{-5}M$) was decreased, 5) With pretreatment of L-arginine($10^{-4}M$), pulmonary arterial relaxation by Ach($10^{-9}-10^{-5}M$) in hypoxia was reversed to the level of relaxation in normoxia. Conclusion: It is concluded that rat pulmonary arterial relaxation by Ach is dependent on the intact endothelium and is largely mediated by NO. Acute hypoxic pulmonary vasoconstriction is related to the suppression on NO formation in the vascular endothelium.

• Journal of Plant Biology
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• v.26 no.4
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• pp.173-180
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• 1983

L-canavanine was added to GAs treated barley seeds, and induced amylase activity, soluble protein content, and arginine content were mesured. Canavanine, added at the beginning of the incubation period, inhibited amylase activity and protein accumulation. Amylase activity decreased markedly by addition of canavanine at 6 hr after incubation, where soluble protein content was not affected. The addition of canavanine after 12 hr incubation did not show serioud inhibited effect on the amylase activity and protein accumulation. GAs incubation caused decrement in arginine content per mg protein, but it was somewhat recovered by canavanine treatment. The longer the time between GAs and canavanine addition was, the less the recovery ration was. Arginine content in the $\alpha$-amylase fraction (ammonium sulfate 20~50% saturation) was lower than in 0~20% fraction, but higher than in 50~80% fraction. These results and control expreiments, using cordycepin and cycloheximide, support the idea that canavanine might incorporate into protein.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.16
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• pp.7031-7038
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• 2015

Background: Arginine may play important roles in tumor progression by providing ornithine for polyamine biosynthesis, required for cell growth. The aim of this work was to determine the expression of arginine metabolic pathway enzymes in head and neck squamous cell carcinoma (HNSCC) in northeast India. Materials and Methods: The expressions of arginase isoforms (ARG1 and ARG2), ornithine aminotransferase (OAT) and ornithine decarboxylase (ODC) were examined in fifty paired HNSCC and adjacent non-tumor tissues by immunohistochemistry. Immunocytochemistry, semiquantitative reverse transcription sq-PCR and quantitative real-time qPCR were used to assess protein and mRNA expressions in peripheral blood of fifty HNSCC patients and hundred controls. Results: ARG1 and ODC protein and mRNA were strongly expressed in peripheral blood from HNSCC patients. No ARG2 expression was observed. In vivo, expression of ARG1, ARG2 and ODC was significantly higher in tumor than in non-tumor tissues. Most tumors expressed low levels of OAT, with no difference in tissues or blood, compared to controls. The absolute extent of maximal ARG1 upregulation with qPCR showed 6.23 fold increase in HNSCC. Conclusions: These findings strongly suggest that in HNSCCs, the ARG1 pathway is stimulated leading to the formation of polyamines as indicated by higher ODC expression, which promote tumor growth.

• Archives of Pharmacal Research
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• v.21 no.6
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• pp.657-663
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• 1998

The enzyme responsible for the synthesis of nitric oxide (NO) from L-arginine in mammalian tissues is known as nitric oxide synthase (NOS) (EC.1.14.13.39). In the present study, the role of NO in the regulation of exocrine secretion was investigated in rat pancreatic acinar cells. Treatment of rat pancreatic acinar cells with cholecystokinin-octapeptide (CCK-OP) resulted in an increase in the arginine conversion to citrulline, the amount of $NO_X$, the release of amylase, and the level of CGMP. Especially, CCK-OP-stimulated increase of arginine to citrulline transformation, the amount of $NO_X$, and CGMP level were completely counteracted by the inhibitor of NOS, NG-monomethyl-L-arginine (MMA), by contrast, that of amylase release was partially reduced. Furthermore, MMA-induced decrease of NOS activity and amylase release showed dose-dependent pattern. The data on the time course of CCK-OP-induced citrulline formation and CGMP rise indicate that NOS and guanylate cyclase were activated by treatment of CCK-OP. However, the mechanism of agonist-stimulated guanylate cyclase activation in acinar cells remains unknown. Therefore, activation of NOS is one of the early events in receptor-mediated cascade of reactions in pancreatic acinar cells and NO, not completely, but partially mediate pancreatic enzyme exocrine secretion.