• The Korean Journal of Physiology
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• 제11권2호
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• pp.9-16
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• 1977

The present experiment was conducted to see whether or not several cardioactive agents influence the 'regenerative $Ca^{++}$ release' in the mechanically disrupted cardiac cells. The mechanically disrupted cardiac cells were prepared by the method of Kerrick and Best from the ventricle of rat. The tension development of the disrupted cardiac cells was measured with a mechanoelectric transducer (RCA 5734). The results were summarized as follows 1) 2 mM caffeine enhanced the regenerative $Ca^{++}$ release, whereas 2 mM Procaine inhibited the $Ca^{++}$ release as reported by other investigators. 2) Epinephrine at concentrations of $10^{-7},\;10^{-6}\;and\;10^{-5}M$ increased the regenerative $Ca^{++}$ release significantly but showed a poor dose response on the $Ca^{++}$ release. 3) Propranolol showed no effect on the regenerative $Ca^{++}$ release when studied alone. Furthermore, it showed no antagonistic effect on an increased regenerative $Ca^{++}$ release induced by epinephrine. 4) Other cardioactive agents such as acetylcholine, ouabain, isoproterenol and c-AMP at concentrations of $10^{-6}M$ showed no effect on the regenerative $Ca^{++}$ release. From the above results, it may be concluded that the cardioactive actions of these agents are not related directly to the process of regenerative $Ca^{++}$ release.

• 한국유기농업학회지
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• 제5권1호
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• pp.79-85
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• 1996

This experiment was carried out to investigate the effect of slow-release fertilizers on yield of radigh. Fertilizers were treated with CDU, MEISTER, Jobi Gohyungbok-hapbiryo, Kyungki Wonyebokbi 1ho, Kyungkibokbi Nojeok, Kyungki Jeonjakgo-hyungbokbi, Tradidtional manuring, and No maunring. Yields of radish were increased with slow-release fertilizers, CDU and MEISTER were effective to radish shoot, also. But analysis of chemical components of plants and soil were no difference. It was very effect to increase yields of radish, to reduce in number of supplementary manuring and laboring.

• 한국유기농업학회지
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• 제5권2호
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• pp.85-91
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• 1997

This experiment was carried out to investigate the effect of slow-release fertilizers on yield of lettuce. Fertilizers were treated with CDU, MEISTER, Jobi Gohyungbokhapbiryo, Kyungki Wonyebokbi 1ho, Kyungkibokbi Nojeok, Kyungki Jeonjakgohyungbokbi, Traditional manuring, and No manuring. Yields of Spinach was increased with slow-release fertilizers, also. But analysis of chemical components of plants and soil were no difference. It was very effect to increase yields of lettuce, to reduce in number of supplementary manuring and laboring.

• 한국환경과학회지
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• 제16권11호
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• pp.1271-1277
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• 2007

This study was conducted to investigate the ratios of phosphorus release to COD uptake, phosphorus release to nitrate removal, and phosphorus uptake to phosphorus release by DNPAOs(denitrifying phosphate accumulating organisms). In case $I{\sim}IV$, influent 1 were fed with synthetic wastewater with influent 2 $NO_3^--N$ injection to anoxic zone and the case V were fed with municipal wastewater with side stream oxic zone instead of influent 2 $NO_3^--N$ injection. As a result, the ratio of phosphorus release to carbon uptake was increased in accordance with nitrate supply. The DNPAOs simultaneously took up phosphate and removed nitrate from the anoxic reactor. In case $I{\sim}IV$, with above 20 mg/L of sufficient $NO_3^--N$ supply, phosphate was taken up excessively by the DNPAOs in anoxic condition. The large amount of both uptake and release of phosphorus occurred above 20 mg/L of nitrate supply, achieving the ratio of phosphorus uptake to phosphorus release to be 1.05. In case V, phosphate luxury uptake was not occurred in system due to 6.98 mg/L of insufficient $NO_3^--N$ supply and the ratio of phosphorus uptake to phosphorus release was 0.98. Consequently, if nitrate as the electron acceptor was sufficient in anoxic zone, the ratio was found to be high.

• Animal cells and systems
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• 제7권4호
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• pp.309-315
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• 2003

Renal dipeptidase (RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19) has been widely studied since it was first purified from porcine kidney brush border membrane. It was reported that RDPase activity in urine samples of acute and chronic renal failure patients decreases. Nitric oxide (NO) is a highly reactive free radical involved in a number of physiological and pathological processes. NO is able to act in a dual mode, leading either to induction of apoptosis or to blunted execution of programmed cell death. NO inhibited the RDPase release from porcine renal proximal tubules, which could be blocked by L-NAME. Chitosan, the linear polymer of D-glucosamine in $\beta$(1\longrightarrow4) linkage, not only reversed the decreased RDPase release by NO but also increased NO production in the proximal tubule cells. The stimulatory effect of NO on RDPase release from proximal tubules in the presence of chitosan must be different from the previously proposed mechanism of RDPase release via NO signaling pathway. Chitosan stimulated the RDPase release in the proximal tubules and increased RDPase activity to 220% and 250% at 0.1% and 1%, respectively. RDPase release was decreased to about 40% in the injured proximal tubules and was recovered in proportion to the increase of chitosan. Chitosan may be useful in recovery of renal function from $HgCl_2$injury.

• Archives of Pharmacal Research
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• 제22권1호
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• pp.48-54
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• 1999

These studies were designed to examine the differential effect of nitric oxide (NO) and cGMP on glutamate neurotransmission. In primary cultures of rat cerebellar granule cells, the glutamate receptor agonist N-methyl-D-aspartate (NMDA) stimulates the elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), the release of glutamate, the synthesis of NO and an increase of cGMP. Although NO has been shown to stimulate guanylyl cyclase, it is unclear yet whether NO alters the NMDA-induced glutamate release and ${[Ca^{2+}]}_i$ elevation. We showed that the NO synthase inhibitor, NG-monomethyl-L-arginine (NMMA), partially prevented the NMDA-induced release of glutamate and elevation of ${[Ca^{2+}]}_i$ and completely blocked the elevation of cGMP. These effects of NO on glutamate release and [Ca2+]i elevation were unlikely to be secondary to cGMP as the cGMP analogue, dibutyryl cGMP (dBcGMP), did not suppress the effects of NMDA. Rather, dBcGMP slightly augmented the NMDA-induced elevation of ${[Ca^{2+}]}_i$ with no change in the basal level of glutamate or ${[Ca^{2+}]}_i$. The extracellular NO scavenger hydroxocobalamine prevented the NMDA-induced release of glutamate providing indirect evidence that the effect of NO may act on the NMDA receptor. These results suggest that low concentration of NO has a role in maintaining the NMDA receptor activation in a cGMP-independent manner.

• Toxicological Research
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• 제12권2호
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• pp.195-201
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• 1996

Endotoxic shock causes death in humans and animals via extreme hypoperfusion of peripheral organs. A massive production of nitric oxide (NO) both from the endothelical cells and smooth muscle cells has been proposed as a possible mechanism in this process. Since NO attenuated the contractility to vasoconstricting agents such as norepinephrine (NE) by directly acting on the smooth muscle cells, this mechanism was considered mainly as a postsynaptic mechanism. In this research it was investigated whether NO, thus released, also participates in the presynaptic events for the regulation of vascular tone in endotoxic shock. The role of NO was studied by adding NO donors or NO synthase inhibitor $N^\omega $methyl-L-arginine (NMA) in stimulated sympathetic nerves of the mesenteric vascular bed and the Langendorff heart of rats. Sodium nitroprusside (SNP), an NO donor, reduced the pressor responses of isolated mesenteric artery either to electrical stimulation or exogenously administered phenylephrine (PE). In this mesentery, although neither agent influenced NE release, in the presence of the adrenergic $\alpha_2$-receptor antagonist yohimbine, elecrical stimulation-evoked NE release was augumented by SNP. In the heart SNP facilitated the NE release induced by electrical stimulation, while NMA had no effect. From these results it is proposed that there exists a local reflex phenomenon in the junction between the sympathetic nerve terminals and the smooth muscle of resistance blood vessels; by which sympathetic responses are reduced by NO at the postjunctional level while NO facilitates NE release contributing to augumentation of sympathetic tone. All these facts suggest that NO produced during endotoxic shock has dual effects: whereas NO blunts the vasoconstrictive activity of NE at the postsynaptic level, NO presynaptically facilitates the release of NE from sympathetic nerve terminals.

• 대한환경공학회지
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• 제29권9호
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• pp.1003-1012
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• 2007

호수 퇴적물의 용출로 인한 수질오염을 예측하고 퇴적 위치에 따른 용출 특성을 파악하기 위해 환경 조건에 따른 용출 차이를 분석하였다. 분석 항목으로는 질소계열, 인계열, COD를 분석하였으며, 모든 시료의 분석 방법은 호수 내부수의 염도가$(Cl^-)$ 2,000 ppm 이상이므로 해수 수질공정 시험법에 준하여 실시하였다. COD는 혐기조일 경우 A지점에서 C지점으로 갈수록 용출율이 증가한 반면, 호기조일 경우 증 감의 경향성이 없었다. $NH_3$-N의 호기조일 경우 A지점에서 C지점으로 갈수록 용출율이 감소하였고, 반대로 질산화 작용으로 인해 $NO_3$-N과 T-N은 A지점에서 C지점으로 갈수록 용출율이 증가하였다. $NH_3$-N, $NO_3$-N의 혐기조는 A지점에서 C지점으로 갈수록 용출율이 증가하였으나 탈질화 작용으로 인하여 T-N의 용출율은 감소하는 경향을 보였다. $PO_4$-P, T-P의 경우 호기조에서 B지점의 용출율이 가장 낮았으며, 이는 용존 산소의 함량이 많아 무기물이 산화되면서 인의 용출이 억제된 것으로 판단된다. $PO_4$-P의 혐기조일 경우 A지점부터 C지점의 용출율이 서로 유사하였다. COD와 $NO_3$-N의 경우 혐기조보다 호기조에서 용출율이 높았으며, 그 외의 항목에서는 호기조보다 혐기조에서 용출율이 높았다.

• The Korean Journal of Physiology and Pharmacology
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• 제1권6호
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• pp.673-679
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• 1997

It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced $[^3H]norepinephrine([^3H]NE)$ release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from $Mg^{2+}-free$ artificial cerebrospinal fluid, induced significant release of $[^3H]NE$ from cortex slices. This ischemia-induced $[^3H]NE$ release was significantly attenuated by glutamatergic neurotransmission modifiers. $N^G-nitro-L-arginine$ methyl ester(L-NAME), $N^G-monomethyl-L-arginine$ (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked $[^3H]NE$ release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited $[^3H]NE$ release dose-dependently. Ischemia-evoked $[^3H]NE$ release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked $[^3H]NE$ release is mediated by NMDA receptors, and activation of NO system is involved.

• The Korean Journal of Physiology and Pharmacology
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• 제3권4호
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• pp.393-404
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• 1999

We have reported that hypoxia stimulates EDRF(s) release from endothelial cells and the release may be augmented by previous hypoxia. As a mechanism, it was hypothesized that reoxygenation can stimulate EDRF(s) release from endothelial cells and we tested the hypothesis via bioassay experiment. In the bioassay experiment, rabbit aorta with endothelium was used as EDRF donor vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin $F_{2a}\;(3{\times}10^{-6}\;M)$ which was added to the solution perfusing through the aorta. Hypoxia was evoked by switching the solution aerated with 95% $O_2/5%\;CO_2$ mixed gas to one aerated with 95% $O_2/5%\;CO_2$ mixed gas. Hypoxia/reoxygenation were interexchanged at intervals of 2 minutes (intermittent hypoxia). In some experiments, endothelial cells were exposed to 10-minute hypoxia (continuous hypoxia) and then exposed to reoxygenation and intermittent hypoxia. In other experiments, the duration of reoxygenation was extended from 2 minutes to 5 minutes. When the donor aorta was exposed to intermittent hypoxia, hypoxia stimulated EDRF(s) release from endothelial cells and the hypoxia-induced EDRF(s) release was augmented by previous hypoxia/reoxygenation. When the donor aorta was exposed to continuous hypoxia, there was no increase of hypoxia-induced EDRF(s) release during hypoxia. But, after the donor aorta was exposed to reoxygenation, hypoxia-induced EDRF(s) release was markedly increased. When the donor aorta was pretreated with nitro-L-arginine $(10^{-5}$ M for 30 minutes), the initial hypoxia-induced EDRF(s) release was almost completely abolished, but the mechanism for EDRF(s) release by the reoxygenation and subsequent hypoxia still remained to be clarified. TEA also blocked incompletely hypoxia-induced and hypoxia/reoxygenation-induced EDRF(s) release. EDRF(s) release by repetitive hypoxia and reoxygenation was completely blocked by the combined treatment with nitro-L-arginine and TEA. Cytochrome P450 blocker, SKF-525A, inhibited the EDRF(s) release reversibly and endothelin antgonists, BQ 123 and BQ 788, had no effect on the release of endothelium-derived vasoactive factors. Superoxide dismutase (SOD) and catalase inhibited the EDRF(s) release from endothelial cells. From these data, it could be concluded that reoxygenation stimulates EDRF(s) release and hypoxia/reoxygenation can release not only NO but also another EDRF from endothelial cells by the production of oxygen free radicals.