• The Korean Journal of Pharmacology
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• v.2 no.1 s.2
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• pp.5-12
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• 1966

In this study the influence of Bradykinin, a biogenic polypeptide, on the excretory function of the dog kidney was investigated, utilizing the clearance and stop-flow method. The results are summarized as follows; 1) Bradykinin administered intravenously elicited a marked antidiuresis. 2) When given into the renal artery, however, prompt increase of the urine flow, sodium excretion and free water clearance without significant change in the glomerular filtration rate ensued. 3) It was also effective during an osmotic diuresis with 10% Mannitol infusion, though the response was not so marked. 4) The stop-flow experiment showed that sodium reabsorption in the proximal tubules is inhibited by the infusion of bradykinin into the renal artery. It was thus concluded that the diuretic effect of bradykinin given intra-arterially results from the inhibition of sodium transport in the proximal tubules.

• Archives of Pharmacal Research
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• v.25 no.1
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• pp.80-85
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• 2002

The incubation of porcine renal proximal tubules (PTs) resulted in the release of the Glycosylphosphatidylinositol (GPI)-anchored renal dipeptidase (RDPase, EC 3. 4. 13. 19) from the membrane after a lag period of approximately 6 hours. This spontaneous release of RDPase from the membrane was inhibited by antibiotics. When the incubation supernatant was added back to fresh PTs, both the antibiotic inhibition of RDPase release and the lag period disappeared. The released RDPase reacted with an anti-cross reacting determinant antibody indicating the presence of the Ins (1, 2-cyc)P. These results suggest that bacteria in the PTs, when incubated, grow find Secrete a phosphatidylinmsitol-specific phospholipase C (PIPLC). This enzyme then hydrolyses the GPI-anchored RDPase and is transferable. RDPase was purified following its release from the membrane by this simple and inexpensive method which may also be applied to other GPI-anchored proteins.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.120-131
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• 2010

Renal tubular acidosis (RTA) is a metabolic acidosis due to impaired excretion of hydrogen ion, or reabsorption of bicarbonate, or both by the kidney. These renal tubular abnormalities can occur as an inherited disease or can result from other disorders or toxins that affect the renal tubules. Disorders of bicarbonate reclamation by the proximal tubule are classified as proximal RTA, whereas disorders resulting from a primary defect in distal tubular net hydrogen secretion or from a reduced buffer trapping in the tubular lumen are called distal RTA. Hyperkalemic RTA may occur as a result of aldosterone deficiency or tubular insensitivity to its effects. The clinical classification of renal tubular acidosis has been correlated with our current physiological model of how the nephron excretes acid, and this has facilitated genetic studies that have identified mutations in several genes encoding acid and base ion transporters. Growth retardation is a consistent feature of RTA in infants. Identification and correction of acidosis are important in preventing symptoms and guide approved genetic counseling and testing.

• The Korean Journal of Physiology
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• v.29 no.1
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• pp.69-80
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• 1995

Renal proximal tubular hypertrophy and hyperfunction are known to be early manifestations of experimental and human diabetes. As the hypertrophy and hyperfunction have been suggested to be central components in the progression to renal failure, an understanding of their underlying causes is potentially important for the development of therapy. A primary rabbit kidney proximal tubule cell culture system was utilized to evaluate the possibility that the renal proximal tubular hypertrophy and hyperfunction observed in vivo in diabetes mellitus, can be attributed to effects of elevated glucose levels on membrane transport systems. Primary cultures of rabbit proximal tubules, which achieved confluence at 10 days, exhibited brush-border characteristics typical of proximal tubular cells. Northern analysis indicated $2.2{\sim}2.3$ and 2.0 kb Na/glucose cotransporter RNA species appeared in fresh and cultured proximal tubule cells after confluence, repectively. The cultured cells showed reduced Na/glucose cotransporter activity compared to fresh proximal tubules. Primary cultured proximal tubule cells incubated in medium containing 20 mM glucose have reduced ${\alpha}-MG$ transport compared to cells grown in 5 mM glucose. In the proximal tubule cultures incubated in medium containing 5 mM or 20 mM glucose, phlorizin at 0.5 mM inhibited 0.5 mM ${\alpha}-MG$ uptake by 84.35% or 91.85%, respectively. The uptake of 0.5 mM ${\alpha}-MG$ was similarly inhibited by 0.1 mM ouabain (41.97% or 48.03% inhibition was observed, respectively). In addition, ${\alpha}-MG$ uptake was inhibited to a greater extent when $Na^{+}$ was omitted from the uptake buffer (81.86% or 86.73% inhibition was observed, respectively). In cell homogenates derived from the primary cells grown in 5 mM glucose medium, the specific activity of the Na/K-ATPase $(6.17{\pm}1.27\;{\mu}mole\;Pi/mg\;protein/hr)$ was 1.56 fold lower than the values in cell homogenates treated with 360 mg/dl D-glucose, 20 mM $(9.67{\pm}1.22\;{\mu}mole\;Pi/mg\;protein/hr)$. Total $Rb^{+}$ uptake occurred at a significantly higher rate (1.60 fold increase) in primary cultured rabbit kidney proximal tubule cell monolayers incubated in 20 mM glucose medium $(10.48{\pm}2.45\;nM/mg\;protein/min)$ as compared with parallel cultures in 5 mM glucose medium. $Rb^{+}$ uptake rate in 5 mM glucose medium was reduced by 28% when the cultures were incubated with 1 mM ouabain. The increase of the $Rb^{+}$ uptake by rabbit kidney proximal tubule cells in 20 mM glucose could be attributed primarily to an increase in the rate of ouabain-sensitive $Rb^{+}$ uptake $(5\;mM\;to\;20\;mM;\;4.68{\pm}0.85\;to\;8.38{\pm}1.37\;nM/mg\;protein/min)$. In conclusion, the activity of the renal proximal tubular Na,K-ATPase is elevated in high glucose concentration. In contrast, the activity of the Nafglucose cotransport system is inhibited.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.3
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• pp.187-191
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• 2003

$Na^+/H^+$ exchanger (NHE) has a critical role in regulation of intracellular pH (pHi) in the renal proximal tubular cells. It has recently been shown that dopamine inhibits NHE in the renal proximal tubules. Nevertheless, there is a dearth of information on the effects of long-term (chronic) dopamine treatment on NHE activities. This study was performed to elucidate the pHi regulatory mechanisms during the chronic dopamine treatments in renal proximal tubular OK cells. The resting pHi was greatly decreased by chronic dopamine treatments. The initial rate and the amplitude of intracellular acidification by isosmotical $Na^+$ removal from the bath medium in chronically dopamine-treated cells were much smaller than those in control. Although it seemed to be attenuated in $Na^+$-dependent pH regulation system, $Na^+$-dependent pHi recovery by NHE after intracelluar acid loading in the dopamine-treated groups was not significantly different from the control. The result is interpreted to be due to the balance between the stimulation effects of lower pHi on the NHE activity and counterbalance by dopamine. Our data strongly suggested that chronic dopamine treatment increased intrinsic intracellular buffer capacity, since higher buffer capacity was induced by lower resting pHi and this effect could attenuate pHi changes under extracellular $Na^+$-free conditions in chronically dopamine-treated cells. Our study also demonstrated that intracellular acidification induced by chronic dopamine treatments was not mediated by changes in NHE activity.

• Journal of the Korean Society of Food Science and Nutrition
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• v.34 no.7
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• pp.968-972
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• 2005

The purpose of this study was to evaluate the effects of chitosan, which is deacetylated derivative of chitin, on the renal function. Renal dipeptidase (RDPase, membrane dipeptidase, dehydropeptidase 1, EC 3.4.13.19) is glycosyl phosphatidyl-inositol (GPI)-anchored ectoenzyme of renal proximal tubular microvilli and was related with renal disease including acute renal failure, pyelitis and nephritis. The released RDPase and Udpase activities were assayed by modified fluorometric method. In vitro experimental groups were consisted of group 1, the concentration ranges of 0, 0.01, 0.05 and $0.1\%$ chitosan only, group 2, the concentration ranges of 1, 2 and 4 mM glycerol only, and group 3, the concentration ranges of 0, 0.01, 0.05 and $0.1\%$ chitosan in the presence of glycerol (4 mM). In vivo experimental groups were consisted of group 1 in which rats were treated with glycerol for the purpose of glycerol-induced renal damage, and group 2 in which rats were treated with chitosan plus glycerol. The RDPase release of 0.01, 0.05, and $0.1\%$ chitosan groups were increased in the concentration dependent manner. The RDPase release of 1, 2, and 4mM glycerol groups were decreased in the concentration dependent manner. Chitosan in the presence of glycerol restored the released RDPase activity in the proximal tubules. In vivo, chitosan inhibited the decrease of RDPase release by glycerol in the kidney and blocked the decrease of Udpase activity by glycerol in urine. These results indicated that chitosan was possible as a functional food to control renal function and its diseases.

• The Journal of Korean Medicine
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• v.17 no.2 s.32
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• pp.133-144
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• 1996

This study investigated the effect of InJinORyungSan on the nephrotoxicity in rat treated with cyclosporin A. Control group were injected with cyclosporin A alone. whereas test group were injected with cyclosporin A and InJinORyungSan extract. In the control group, blood urea nitrogen(BUN), serum creatinine(S-Cr) and renal lipid peroxidation(LPO) level were significantly increased, but renal superoxide dismutase(SOD) activity was significantly decreased. In the kidney of control group, the destruction of distal convoluted tubules(DCT) and proximal convoluted tubules(PCT) were observed in renal cortex, lymphocytes and fibroblast were appeared in the portion of DCT destruction. However, in the test group, BUN, S-Cr and renal LPO level were significantly decreased as compared with control group, on the other hand, renal SOD activity was significantly increased. In the kidney of test group, the destruction of DCT and PCT were repaired as compared with control group. These results demonstrated that InJinORyungSan. can be attributed to recovery from nephrotoxicity, We consider that activated SOD by InJinORyungSan suppress renal LPO or production of free radicals induced by cyclosporin A.

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.212.3-213
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• 2001

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.213.1-213.1
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• 2001

• The Journal of Internal Korean Medicine
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• v.18 no.1
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• pp.147-155
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• 1997

This study was undertaken to determine whether Salviae-radix (SVR) exraction exerts benefical effect against oxidant-induced inhibition of tetraethylammonium (TEA) uptake which is actively secreted by renal proximal tubules. TEA uptake increased as function of incubation time to 60 min. When renal cortical slices were exposed to 50 mM $H_2O_2$, TEA uptake was significantly inhibited. The inhibition was significantly protected by addition of 0.5% SVR extraction. The benefical effect of SVR was dose-dependent over the concentration range of 0.1-1%; $H_2O_2$ (50 mM)-induced inhibition of TEA uptake was completely protected by 0.5-1% SVR extraction. $H_2O_2$ increased LDH release which was accompanied by an increase in lipid peroxidation in renal cortical slices. These changes were prevented by 0.5% SVR. These results suggest that SVR exerts benefical effect against oxidant-induced impairment of membrane transport function, this effect may be due to by an antioxidant action.