• Proceedings of the KSAR Conference
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• 2001.03a
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• pp.88-88
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• 2001

소 난포란을 체외에서 성숙, 수정시킨 후, 2~8 세포기 수정란을 체외배양액인 CR$_1$aa에 일정량의 nitric oxide scavenger, Hb와, inhibitor인 L-nitro - L- arginine methyl ester (L-NAME)를 첨가 배양하여 체외발육에 미치는 영향을 검토하고자 실시하였다. 체외수정 후 체외배양 48시간에 난구세포의 제거 유.무에 따라 CR$_1$aa 배양액에 hemoglobin을 0, 1, 5$\mu\textrm{g}$/$m\ell$를 첨가한 구의 상실배기이상 체외발육성적은 난구세포를 제거한 구에서 23.8%, 33.3% 및 26.8%였으며, 난구세포를 제거하지 않은 구에서는 각각 39.5%, 54.8% 및 48.8%로써 난구세포를 제거하지 않은 구에 Hb를 1$\mu\textrm{g}$/$m\ell$를 첨가한 구가 여타구 보다 통계적으로 높은 결과를 얻었다(P<0.05). 체외수정 후 체외배양 96시간 후 난구세포를 제거 유.무에 따라 Hb를 0, 1, 5$\mu\textrm{g}$/$m\ell$를 첨가하였을 때, 상실배기 이상 체외발육성적은 난구세포를 제거한 구에서 각각 28.6%, 46.2% 및 39.1%였으며, 난구세포를 제거하지 않은 구에서는 각각 33.9%, 67.2% 및 46.0%로써, 난구세포를 제거하지 않은 구에 Hb를 1$\mu\textrm{g}$/$m\ell$첨가구가 여타구에 비해 통계적으로 유의하게 높게 나타났다( P<0.05).CR$_1$aa배양액에 L-NAME를 0, 10, 50 및 100mM을 첨가한 구에서 상실배이상 발육된 체외발육성적은 각각 55.6%, 64.9%, 58.8% 및 66.7%로써 L-NAME 첨가구가 무첨가구에 비해 커다란 차이가 나타나지 않았다(P>0.05). 본 실험의 결과로 볼 때, nitric oxide scavenger인 hemoglobin의 첨가는 체외수정 후 체외배양 96시간에 1$\mu\textrm{g}$/$m\ell$ 첨가하는 것이 체외수정란의 체외 발육율을 향상시켰으며, nitric oxide inhibitor인 L-NAME는 첨가 농도에 관계없이 체외수정란의 체외발육율에 영향을 미치지 않는 것으로 나타났다. 본 실험에서 생산된 배반포기 체외수정란의 세포수에는 커다란 차이가 인정되지 않았다.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.197-202
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• 1994

The present study was aimed to determine if endogenous L-arginine-nitric oxide (NO) pathway has central, rather than peripheral, mechanisms in blood pressure regulation. Arterial blood pressure and heart rate responses to acute inhibition of the t-arginine-NO pathway were examined in rats anesthetized with thiopental (50 mg/kg, IP). An intracerebroventricular (ICV) cannula was placed in the left lateral ventricle. The right femoral artery was cannulated to measure arterial blood pressure and the vein to serve as an infusion route. $N^G-nitro-L-arginine$ methyl ester (L-NAME) was infused either intracerebroventricularly or intravenously. ICV infusion $(1.25\;{\mu}L/min)$ of L-NAME $(20\;or\;100\;{\mu}g/kg)$ per minute for 60 min) increased the mean arterial pressure and heart rate. Plasma renin concentrations(PRC) were significantly lower in L-NAME-infused group than in the control. L-Arginine $(60\;{\mu}g/min,\;ICV)$ prevented the pressor response to ICV L-NAME. The pressor response was not affected by simultaneous intravenous infusion of saralasin, but was abolished by hexamethonium treatment. Intravenous infusion $(40\;{\mu}L/min,\;10{\sim}100\;{\mu}g/kg\;per\;minute\;for\;60\;min)$ also increased blood pressure, while it decreased heart rate. These results indicate that endogenous L-arginine-NO pathway has separate central and peripheral mechanisms in regulating the cardiovascular function. The central effect may not be mediated via activation of renin-angiotensin system, but via, at least in part, activation of the sympathetic outflow.

• Parasites, Hosts and Diseases
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• v.33 no.4
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• pp.399-400
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• 1995

Neoniplostomun seoulense is the emended name for IV. seoulenis because of the Latin grammar for corresponding suffix of the species name in scientific nomenclature.

• Biomolecules & Therapeutics
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• v.8 no.2
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• pp.113-118
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• 2000

TEA, glibenclamide, L-NAME and SKF 525A-induced reversible contraction were investigated using acetylcholine, sodium nitroprusside (SNP) and pinacidil in rat abdominal and thoracic aorta. Acetylcho-line, SNP or pinacidil produced in a dose dependent manner relaxation on phenylephrine-induced contraction In rat aorta. TEA, SKF 525A, and L-NAME produced reversible contractions on acetylcholine-induced relaxation, but not on SNP- or pinacidil-induced relaxation. Glibenclamide significantly produced reversible con- traction on pinacidll-induced relaxation. The reversible effect of TEA on the acetylcholine-induced relaxation was reduced by SKF 525A. These results indicate that the acetylcholine-induced relaxation may be mediated by NO, cytochrome P$_{450}$-dependent epoxygenase pathway, or $Ca^{2+}$ activated $K^{+}$ channel, and the pinacidil-induced relaxation may be mediated by ATP-sensitive $K^{+}$ channel.annel.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.5
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• pp.369-378
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• 2000

This study was undertaken to investigate an involvement of nitroxergic innervation in gastric smooth muscle of rat. Isometric tension study, the measurement of single cell length, NADPH diaphorase stain of smooth muscle layers and neuronal nitric oxide synthase (nNOS) western blotting were performed. Sodium nitroprusside (SNP), a nitric oxide donor, relaxed the muscle strips precontracted by acetylcholine (ACh) in a concentration-dependent manner. Pretreatment of L-arginine decreased the contraction induced by electric field stimulation (EFS). Pretreatment of $N^G-nitro-L-arginine$ methyl ester (L-NAME), a NOS inhibitor, increased the EFS-induced contractions. LY 83583, a guanylate cyclase (GC) inhibitor, reversed the inhibitory actions of L-arginine on the muscle contractions. The effects of L-Arginine, L-NAME and LY 83583 on ACh-induced contractions were not significant. L-arginine reduced the EFS-induced contraction in circular muscle, whereas L-NAME enhanced the EFS-induced contraction in longitudinal strips. By EFS, the phasic contractions appeared approximately $20{\sim}25$ seconds later. L-NAME significantly shortened the delay time to about $2{\sim}3$ seconds. In single cell study, ACh contracted gastric smooth muscle cells, SNP relaxed the cells, and the latter also inhibited the ACh-induced contraction. LY 83583 enhanced the ACh-induced contraction and antagonized SNP-induced relaxation. NADPH diaphorase activity was assessed by a histochemistry, nitroblue tetrazolium (NTB) staining. Positive staining was observed in both circular and longitudinal muscle layers. L-arginine increased the staining, while L-NAME decreased the staining. Western blotting for nNOS proved the presence of nNOS in rat gastric smooth muscle. EFS and additional $Ca^{2+}$ increased nNOS protein expression. These results suggest that in rat stomach, both circular and longitudinal muscle layers are innervated with nitroxergic nerves which relax the gastric smooth muscle via NO-cGMP pathway.

• Korean Journal of Ichthyology
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• v.35 no.2
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• pp.136-140
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• 2023

A single opah specimen (705 mm SL) was collected from Samcheok, South Korea on November, 2014, and firstly reported as Lampris guttatus by Jeong et al. (2015). Thereafter Lampris lauta was revived and three additional species (Lampris australensis, Lampris incognitus, Lampris megalopsis) were newly reported (Underkoffler et al., 2018). Therefore, it needs to review the scientific name of the Korean opah. The first reported opah specimen from Korea is now preserved as stuffed specimen at the Seodaemun Museum of Natural History in Seoul. We re-investigated the morphological features of stuffed specimen. It was characterized by having the following morphological combinations; orbital diameter is greater than 5% of fork length, whole body including head with white irregular spots, all fins are deep red. In addition, L. guttatus is confined to North Atlantic Ocean, whereas L. megalopsis is distributed worldwide from temperate to tropical waters. Therefore, our comprehensive study suggests that the scientific name of opah (L. guttatus) reported in Korea must be changed to L. megalopsis based on morphological characteristics and distribution area.

• Korean Journal of Veterinary Research
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• v.43 no.4
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• pp.573-578
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• 2003

The effects of removing the endothelium on the vasodilatory response to substance P, calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP) was examined in the isolated rabbit renal artery. The vasodilator response to substance P ($0.1{\mu}M$) was completely absent in vessels in which the endothelium had previously been removed. There was no significant difference in the vasodilatation produced in response to CGRP ($0.1{\mu}M$), or VIP ($0.1{\mu}M$) in the intact and removed-endothelium rabbit renal artery segments. L-NAME ($100{\mu}M$) significantly reduced the vasodilatory response to substance P ($0.1{\mu}M$). This inhibition was significantly attenuated when L-arginine (10 mM) was also present in the organ bath along with L-NAME ($100{\mu}M$). Indomethacin ($1{\mu}M$) did not significantly affect the vasodilatation produced in response to substance P ($0.1{\mu}M$). The inhibitory effect of L-NAME ($100{\mu}M$) and indomethacin ($1{\mu}M$) on the vasodilatory response to substance P ($0.1{\mu}M$) was not significantly different from that produced by L-NAME ($100{\mu}M$) alone. This study indicates that substance P induced vasodilatation via an endothelium-dependent mechanism in the isolated rabbit renal artery. It also established that CGRP and VIP induced vasodilatation by an endothelium-independent mechanism and substance P-induced vasodilatation is at least partially via NO.

• Korean Journal of Veterinary Research
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• v.42 no.3
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• pp.321-326
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• 2002

The effect of nitric oxide synthase(NOS) inhibita, $N^G$-nitro-L-arginine-methyl ester(L-NAME) and prostanoid synthesis inhibiter, indomethacin on the photorelaxation, when was exposed to the long-wave length UV-light, was examined on the precontraction by the phenylephrine in the isolated pig renal artery. 1. UV-light relaxed both with-endothelium and without-endothelium in the pig renal arterial ring contracted by the phenylephrine. The magnitude of photorelaxation was dependent on the exposure time for UV-light. 2. UV-Iight induced relaxation was inhibited by L-NAME and indomethacin on the precontraction by the phenylephrine in the isolated pig renal artery. 3. UV-Iight induced relaxation was inhibited by methylene blue on the precontraction by the phenylephrine in the isolated pig renal artery. These results suggest that UV-light induced photorelaxation may be due to cGMP involved both nitric oxide and prostanoid on the precontraction by the phenylephrine in the isolated pig renal artery.

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.507-515
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• 2005

Melatonin, the principal hormone of the vertebral pineal gland, participates in the regulation of cardiovascular system in vitro and in vivo. However, the effects of melatonin on vascular tissues are still vague. The aim of this study was to assess the relationship between phospholipase C (PLC) and nitric oxide synthase (NOS)/cyclic guanosine 3',5'-monophosphate (cGMP) signaling cascade in the relaxatory action of melatonin in isolated rat aorta. Melatonin induced a concentration-dependent relaxation in phenylephrine (PE)- and KCl-precontracted endothelium intact (+E) aortic rings. In KCl-precontracted +E aortic rings, the melatonin-induced vasorelaxation was not inhibited by endothelium removal or by pretreatment with NOS inhibitors, L-$N^G$-nitor-arginine (L-NNA) and L-$N^G$-nitor-arginine methyl ester (L-NAME), guanylate cyclase (GC) inhibitors, methylene blue (MB) and 1H-[1,2,4] oxadiazolo-[4,3-a] quinoxalin-1-one (ODQ). In PE-precontracted +E aortic rings, the melatonin-induced vasorelaxation was inhibited by endothelium removal or by pretreatment with L-NNA, L-NAME, MB, ODQ and 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC). Moreover, in without endothelium (-E) aortic rings and in the presence of L-NNA, L-NAME, MB and ODQ in +E aortic rings, the melatonin-induced residual relaxations and residual contractile responses to PE were not affected by NCDC, a PLC inhibitor. It is concluded that melatonin can evoke vasorelaxation due to inhibition of PLC pathway through the protein kinase G activation of endothelial NOS/cGMP signaling cascade.

• The Korean Journal of Physiology
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• v.30 no.1
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• pp.33-41
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• 1996

The present study was aimed to investigate the role of endothelium-derived nitric oxide (NO) in the control of renin release and to examine if NO is implicated in the development of two-kidney, one clip (2K1C) hypertension. Male Sprague-Dawley rats $(150{\sim}200\; g)$ were constricted at the left renal artery. They were then supplemented with $N^{G}-nitro-L-arginine\;methyl\;ester\;(L-NAME,\; 5mg/100\;mL)$ or with L-arginine hydrochloride (400 mg/100 mL) in the drinking water. The control group was supplied with normal tap water. The sham-clipped rats were operated as in 2K1C rats except for that no clip was made. The kidneys were taken to examine in vitro release of renin at days 7 and 14 following clipping the renal artery. Northern blot analysis was also done to assess the expression of renin gene in the kidney. In sham-clipped rats, L-NAME caused a sustained increase of the blood pressure, whereas L-arginine was without effect. Neither L-NAME nor L-arginine-supplementation significantly affected the development of hypertension in 2K1C rats. Plasma renin concentration (PRC) measured on day 28 did not significantly differ among the L-NAME, L-arginine and control groups either in 2K1C or in sham-clipped rats. Renin contents (RRC) in the clipped kidney were increased, while those in the contralateral kidney were decreased. The release of renin in vitro from cortical slices was also enhanced in the clipped kidney, whereas it was attenuated in the contralateral. Comparing the RRC and in vitro release, the latter was more rapidly decreased than the former in the contralateral kidney. The renin mRNA levels in the contralateral kidney were almost at their nadir at days 7 and 14 in 2K1C rats. It is suggested that NO does not affect the development of 2K1C hypertension in which the renin-angiotensin system has been activated. The data also confirm that RRC and renin gene expression are increased in the clipped kidney and suppressed in the contralateral kidney in 2K1C rats.