• KOREAN JOURNAL OF CROP SCIENCE
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• v.52 no.2
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• pp.213-219
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• 2007

It has been well established that aluminum (Al) inhibits root tip growth rapidly in acid soil. We report the correlation between Al induced growth inhibition and impaired $H^+-flux$ in mung bean (Vigna radiate L. cv. Kumsung). The root growth inhibition was dependent on Al concentration (0, 10, 25, 50, $100{\mu}M$) and exposure time (12 and 24 h). Using Hematoxylin staining, it was observed that the root damage was occurred preferentially in regions with high Al accumulation. Using the pH indicator, it was shown that the surface pH of root tip was strongly alkalized in the control whereas changed only slightly in the $50{\mu}M$ Al-treated root. The $H^+-ATPase$ activity of plasma membrane vesicles was inhibited by 56% in the Al-treated roots compared to control root. Decrease in the amount of the plasma membrane $H^+-ATPase$ (100 kDa) translation in the plant roots under Al stress was demonstrated by Western blot analysis. These results indicate that the dynamics of $H^+-flux$ across the root tip play an important role in root growth under Al stress.

• The Korean Journal of Physiology
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• v.24 no.2
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• pp.345-352
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• 1990

To determine the role of sulfhydryl group in transport of organic ions across the basolateral membrane of renal proximal tubules, effect of p-chloromercuribenzoic acid (PCMB) on the transport of tetraethylammonium (TEA) and p-aminohippurate (PAH) was studied in rabbit renal cortical slices. PCMB caused irreversible inhibition of TEA and PAH uptake in a dose-dependent manner, with $I_{50}$ value (concentration for 50% inhibition) of $30\;{\mu}M$ for TEA and $75\;{\mu}M$ for PAH. Kinetic analysis of TEA and PAH uptakes showed that PCMB decreased Vmax $(62.35\;vs.\;28.32\;n\;mole/g{\cdot}min\;fur\;TEA:\;385.24\;vs.\;170.36\;n\;mole/g{\cdot}min\;for\;PAH)$ without changing Km. The inhibitory action of PCMB on TEA and PAH uptakes was independent of pH of the pretreatment medium. The inhibitory effect of PCMB on the uptake of TEA or PAH was prevented by dithiothreitol, but not by the substrate. PCMB inhibited Na-K-ATPase activity in a dose-dependent manner with $I_{50}$ value of $50\;{\mu}M$, which is similar to those for TEA and PAH uptake. These results suggest that PCMB inhibits the transport of organic cations and anions in the renal basolateral membrane by directly affecting the SH-group in the transporter molecules or secondly by altering the Na-K-ATPase activity.

• The Korean Journal of Physiology
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• v.18 no.2
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• pp.139-150
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• 1984

Vanadate is a potent inhibitor of Na-K-ATPase. Ouabain, the another specific inhibitor of Na-K-ATPase, induces the contraction in cardiac muscle and smooth muscle. But, some investigators observed the discrepancies between vanadate and ouabain-induced contraction in cardiac muscle. The difference of vanadate and ouabain-induced contraction was investigated in the cat ileal smooth muscle. The following results were obtained. 1) Ouabain-induced contraction was biphasic, but vanadate-induced contraction had one peak. 2) Atropine inhibited ouabain·induced contraction, but did not inhibit vanadate-induced contraction. 3) Changes in external $Ca^{++}$concentration or $Ca^{++}$ antagonists had a greater influence on the contraction induced hy vanadate than by ouabain. 4) Removal of $Na^+$ from incubation medium and high $K^+$ abolished ouabain-induced contraction, but had no effect on vanadate-induced contraction. 5) Vanadate-induced contraction was potentiated in the presence of ouabain. 6) After 3 hrs incubation with vanadate, there was no change in intracellular $Na^+$ concentrations in contrast with ouabain. These results suggest that vanadate contracts ileal smooth muscle through the mechanism different from ouabain, and this is independent of the inhibition of Na-K-ATPase activity.

• The Korean Journal of Physiology
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• v.17 no.1
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• pp.55-61
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• 1983

Effects of SITS (4-acetamido-4'-isothiocyano-2, 2'-disulfonic stilbene) on a $Na^+$ transport, tissue oxygen consumption and Na-K-ATPase activity were studied in isolated frog skin preparations. $Na^+$ transport was estimated by measuring the short-circuit current(SC) across the skin; oxygen consumption was measured in separated epidermis as well as in intact skin; and Na-K-ATPase was assayed in $24,000{\times}g$ fraction of epidermal homogenates. The SCC across the skin Was rapidly and substantially reduced in the presence of 10 mM SITS in the medium bathing the outside(mucosal) surface of the skin. When the drug was added to the inside(serosal) bathing medium, there was about 20 min delay for inhibition of SCC and the effect was less pronounced. The above effect of SITS was independent of the presence of $Cl^-$ in the bathing medium. The oxygen consumption of the skin tissue was not affected by SITS, but the Na-K-ATPase activity of a subcellular fraction of the skin was significantly inhibited. These results suggest that SITS retards $Na^+$ transport across the frog skin primarily by interfering $Na^+$ entry across the mucosal membrance of the epithelial cell, although an effect on $Na^+$ pump can not be ruled out completely.

• The Journal of Internal Korean Medicine
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• v.11 no.2
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• pp.148-169
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• 1990

The Present experiment was designed to investigate the effects of Soo Jeom San on the function of heart and digestive organs. And thus it was analyzed the total acidity, recovery effect, and the other various enzyme activities such as ATPase, Creatine kinase, Aspartate transaminase, and Lactate dehydrogenase. The results were obtained as follows : 1. The Total acidity decreased after Soo JeomSan administration for 6 days, however the total acidity inoreased after the drug administration for 9 days, these phenomena demonstrate that Soo Jeom San acts as a dual factor. The mechanism of decreasing the total acidity was considered to the inhibition of ATPase activity used for HCI active transport from parietal cells. 2. Soo Jeom San recovered the islets of Langerhans which was disrupted by streptozotocin. The recovery mechanism was suggested that Soo Jeom San stimulates the ${\beta}-cell$ proliferation. 3. Soo Jeom San inhibited the enzyme activities such as Creatine kinase and Aspartate transaminase, however the drug activated Lactate dehydrogenase. According to the obtained results, Soo Jeom San may be used for curing gastric ulcer and myocardiac infarction.

• Natural Product Sciences
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• v.23 no.4
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• pp.299-305
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• 2017

P-methoxycinnamic acid and 3,4,5-trimethoxycinnamic acid are the compounds found in Polygalae Radix, the root of Polygala tenuifolia Willdenow, and have been reported to have hepatoprotective and anti-neurodegenerative effects. On the other hand, there are no reports of their effects on gastric lesions. This study examined the inhibitory effects of cinnamic acids, including p-methoxycinnamic acid, 3,4,5-trimethoxycinnamic acid, and 8 compounds (cinnamic acid, 2-(trifluoromethyl) cinnamic acid, 3-(trifluoromethyl) cinnamic acid, trans-4-(trifluoromethyl) cinnamic acid, 4-(dimethylamino) cinnamic acid, 3,4-(methylenedioxy) cinnamic acid and 3,4-dihydroxycinnamic acid), which were selected based on their presence in medicinal herbs and molecular weight, against gastric lesions. Animal models were used to confirm the protective effects on acute gastritis caused by the administration of HCl/EtOH. Gastric acid inhibition was examined by an acid-neutralizing test and the proton pump ($H^+/K^+$-ATPase) inhibiting activity. In addition, antioxidant tests were performed and the gastric emptying rate was determined. The results showed that cinnamic acid, p-methoxycinnamic acid, and 3,4,5-trimethoxycinnamic acid had an inhibitory effect on gastric lesions.

• YAKHAK HOEJI
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• v.31 no.6
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• pp.376-393
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• 1987

This study was performed in order to investigate the effect of nifedipine, a vasodilating drug which acts through calcium antagonism, on renal function using mongrel dog. Nifedipine, when given interavenously in doses ranging from 1.5 to 5.0$\mu\textrm{g}$/kg, elicited diuresis along with less changes of glomerular filtration rate and significant increases of renal plasma flow, so that the filtration fraction(FF) decreased significantly, at the same time both osmolar and free water clearances increased, and amount of sodium, potassium and calcium excreted in urine increased significantly. Nifedipine, when infused into a renal artery in doses from 0.05 to 0.15$\mu\textrm{g}$/kg/min, exhibited identical responses to the actions of intraveneous nifedipine except significant increase of glomerular filtration rate and no change of FF, which was confined only to the infused kidney. The renal action of nifedipine into a renal artery were not influenced by renal denervation, decreased significantly by ouabain, Na$^+$-K$^+$-ATPase inhibitor, which was given into a renal artery. Nifedipine infused into a renal artery in dog pretreated with propranolol i.v. produced diuresis associated with the increase of electrolytes excretion by reduction of electrolyte reabsorption and with no changes of glomerular filtration rate and renal plasma flow. Thus, it is concluded that nifedipine infused into a renal aretery produces diuretic action along with both improvement of hemodynamics and inhibition of electrolytes reabsorption, which may be related to sympathetic $\beta$-receptor or Na$^+$-K$^+$-ATPase activity because the action of nifedipine in kidney is blocked by propranolol or ouabain.

• Journal of Radiation Protection and Research
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• v.15 no.2
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• pp.1-6
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• 1990

An attempt was made to test the possibility of a major role for the $Na^{+}-K^{+}$ adenosine triphosphatase (ATPase)system in the diuresis induced by uranyl nitrate(UN). Fisher 344 rats were intravenously injected with UN(5 mg/kg, 15 mg/kg and 30 mg/kg). Urinary excretion of $Na^{+}\;and\;K^{+}$ significantly increased in 24 h exposure on the UN and then decreased below the normal level 3 days after the treatment. $Na^{+}-K^{+}$ ATPase activity of kidney was significantly inhibited in high dosages of UN 15mg/kg and UN 30 mg/kg 3-5 days after injection. And then the recovery of the enzyme activity was observed within 5-10 days after injection, at which the regeneration of the tubular cells occurred.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.601-609
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• 1998

The present study was undertaken to examine the role of phospholipase $A_2\;(PLA_2)$ in oxidant-induced inhibition of phosphate transport in primary cultured rabbit renal proximal tubule cells. Uptakes of phosphate and glucose were dose-dependently inhibited by an oxidant t-butylhydroperoxide (tBHP), and the significant inhibition appeared at 0.025 mM of tBHP, whereas tBHP-induced alterations in lipid peroxidation and cell viability were seen at 0.5 mM. tBHP stimulated arachidonic acid (AA) release in a dose-dependent fashion. A $PLA_2$ inhibitor mepacrine prevented tBHP-induced AA release, but it did not alter the inhibition of phosphate uptake and the decrease in cell viability induced by tBHP. tBHP-induced inhibition of phosphate transport was not affected by a PKC inhibitor, staurosporine. tBHP at 0.1 mM did not produce the inhibition of $Na^+-K^+-ATPase$ activity in microsomal fraction, although it significantly inhibited at 1.0 mM. These results suggest that tBHP can inhibit phosphate uptake through a mechanism independent of $PLA_2$ activation, irreversible cell injury, and lipid peroxidation in primary cultured rabbit renal proximal tubular cells.

• The Korean Journal of Pharmacology
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• v.24 no.2
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• pp.179-187
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• 1988

Verapamil, tetrodotoxin and tetraethylammonium chloride in the stated amount did not affect the $Na^{++}$ induced $Ca^{++}$ release. $Cd^{++}$ and $Zn^{++}$ significantly inhibited the $Na^{++}$ induced $Ca^{++}$ release. $Mn^{++}$ also inhibited $Na^+-Ca^{++}$ exchange. $Cd^{++}$ inhibited $Na^+-Ca^{++}$ exchange noncompetitively with an apparent inhibition constant (Ki) of $100\;{\mu}M$. $Cd^{++}$ caused loss of sulfhydryl group, whereas $Zn^{++}$ did not show any significant effect. $Cd^{++}$ and $Zn^{++}$ effectively inhibited $Na^+-Ca^{++}$ ATPase and slightly inhibited $Ca^{++}-Mg^{++}$ ATPase. Carbonyl cyanide chlorophenylhydrazone, 2,4-dinitrophenol and sodium arsenate stimulated the $Na^{++}$ induced $Ca^{++}$ release. Dibucaine and oligomycin slightly inhibited it. The results suggest that the $Na^+-Ca^{++}$ exchange on the synaptosomal plasma membrane may be not accomplished by ion channels. The $Na^+-Ca^{++}$ exchange is sensitively inhibited by $Cd^{++}$ and this transport process appears to be partially regulated by sulfhydryl groups of the synaptosomal plasma membrane. It is also postulated that $Na^+-Ca^{++}$ exchange is suppressed during the phosphorylation reaction of protein component on the neuronal membrane.