• 대한수의학회지
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• 제37권1호
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• pp.111-117
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• 1997

This study was carried out determine the effect of renal ischemia on amino acid transport in rabbit renal cortical slices. The animal models of renal ischemia induced experimentally by clamping the renal artery. These results were summarized as follows: 1. The uptake of amino acids lysine and ${\alpha}$-aminobutyrate(AIB), dicarboxylate succinate and organic anion PAH in cortical slices was normal or increased after 30 or 60 min of ischemia in vivo. 2. In a 30 min ischemic kidney, the slice uptake of amino acids was returned to the control level by 30 min of reflow. In a 60 or 90 min ischemic kidney, the lysine uptake was returned to the control level after of reflow, but the uptake of AIB and succinate was significantly reduced during reflow period of 30-120 min. 3. Oxygen consumption in cortical slices was increased after 30 min of ischemia but was not altered by 60 min of ischemia. This results indicat that transient ischemia caused increasing of amino acid uptake in renal cortical slices without metabolic disorder of renal proximal tubule.

• The Korean Journal of Physiology
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• 제21권2호
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• pp.283-289
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• 1987

Uric acid transport across the basolateral membrane of renal proximal tubules was studied in rabbit kidney cortical slices. Uric acid uptake was greater under $O_2$ atmosphere compared to under $N_2$ atmosphere, and was increased with $Na^{2+}$ concentration in incubation medium. Uric acid inhibited PAH uptake but not TEA uptake and did trans-stimulated PAH efflux. PAH also inhibited uric acid uptake. Uric acid uptake was inhibited by harmaline, ouabin, SITS, DIDS and pyrazinoic acid. The inhibition of PAH uptake by these inhibitors also was reasonably comparable to that of uric acid uptake. These results suggest that uric acid was transported across the basolateral membrane of renal tubule by a carrier-mediated process which was by a common transport system with PAH in rabbit.

• The Korean Journal of Physiology
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• 제25권2호
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• pp.171-177
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• 1991

This study was carried out to determine effect of acute renal ischemia on transport function of organic cation, tetraethylammonium (TEA), in rabbit kidney proximal tubule. Clamping of the renal artery for 30 and 60 min produced a polyuria which was accompanied by an increase in $Na^+$ excretion. The capacity of kidney cortical slices to accumulate TEA was increased after 30 and 60 min of ischemia. When blood flow was restored for 30 min after 30 and 60 min of ischemia, the augmented TEA uptake was recovered to the control values. Oxygen consumption of cortical slices was stimulated after 30 min of ischemia, whereas it was not altered by 60 min of ischemia. A 90-min ischemia produced a significant inhibition of TEA uptake and tissue oxygen consumption. These results suggest that the basolateral transport system for organic cation persists after ischemic periods of 60 min despite evidence that tubular reabsorptive mechanism of $Na^+$ and water is markedly impaired. This may indicate that the active secretory systems of proximal tubule are more resistant to ischemic injury than the reabsorptive systems.

• 대한의생명과학회지
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• 제8권4호
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• pp.251-256
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• 2002

This study was undertaken to determine the underlying mechanisms of reactive oxygen species-induced cell injury in renal epithelial cells and whether there is a difference in the role of lipid peroxidation between freshly isolated renal cells and cultured renal cells. Rabbit renal cortical slices were used as a model of freshly isolated cells and opossum kidney (OK) cells as a model of cultured cells. Cell injury was estimated by measuring lactate dehydrogenase (LDH) release in renal cortical slices and frypan blue exclusion in OK cells. $H_2O$$_2$ was used as a drug model of reactive oxygen species. $H_2O$$_2$ induced cell injury in a dose-dependent manner in both cell types. However, renal cortical slices were resistant to $H_2O$$_2$ approximately 50-fold than OK cells. $H_2O$$_2$-induced cell injury was prevented by thiols (glutathione and dithiothreitol) and iron chelators (deferoxamine and phenanthroline) in both cell types. $H_2O$$_2$-induced cell injury in renal cortical slices was completely prevented by antioxidants N,N-diphenyl-p -phenylenediamine and Trolox, but the cell injury was not affected by these antioxidants in OK cells. $H_2O$$_2$ increased lipid peroxidation in both cell types, which was completely inhibited by the antioxidants. These results suggest that $H_2O$$_2$ induces cell injury through a lipid peroxidation-dependent mechanism in freshly isolated renal cells, but via a mechanism independent of lipid peronidation in cultured cells.

• 한국임상수의학회지
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• 제24권3호
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• pp.392-399
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• 2007

Scutellaria baicalensis Georgi. (SBGE) is known to be antioxidant effect. In addition of the effects, we further investigated the SBGE on the antioxidant effect on a renal cortical slices cell and kidney protecting effects. The results were as follows. 1 When renal cortical slices separated from a rabbit's kidney were treated with 1mM tert-Butylhydroperoxide (t-BHP) in the presence of SBGE. SBGE significant prevented t-BHP induced increase in lactate dehydrogenase (LDH) release and lipid peroxidation. 2. When renal cortical slices separated from a rabbit's kidney were treated with oxidant $300{\mu}M$ cisplatin in the presence of SBGE. SBGE significant prevented cisplatin-induced increase in LDH release and lipid peroxidation. 3. Pretreatment with 0.1g/kg SBGE for seven day and treatment with 5 mg/kg cisplatin by the intraperitoneal injection The results were that the pretreatment group with SBGE showed a significant decrease in lipid peroxidation, increase in clearance rate of blood urea nitrogen (BUN) and creatinine in the kidney than the administering single agent group of cisplatin. and pretreatment group with SBGE showed intact microvillus of proximal tubule and no contraction of rumen, it was a similar result with normal group. With the results SBGE showed to be highly effective on antioxidant effect and cellular protection activity against cisplatin that was a toxic agent on a kidney. Therefore, SBGE is considered to have protective effective on a disordered kidney or kidney diseases such as nephritis or renal failure that cause tissue damages in a kidney.

• The Korean Journal of Physiology
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• 제19권1호
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• pp.49-59
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• 1985

The effects of anions on net accumulation of $(\rho-aminohippuric\;acid)$(PAH) were studied in rabbit kidney cortical slices. Experiments were carried while varying the major anionic composition of the incubation medium(replacement of $Cl^-$ by isethionate and $SCN^-$). The total replacement of $Cl^-$ with isethionate, $SO_4\;^{2-}$ and $SCN^-$ in the incubation medium decreased the 60-min slice-to-medium concentration(S/M) ratio of PAH to 60%, 40% and 50% of control value, respectively. The degree of inhibition in PAH accumulation by the replacement of isethionate and $SCN^-$ was increased with increasing of both preincubation and incubation time. The influence of isethionate and $SCN^-$ on PAH uptake was fully reversible. Both isethionate and $SCN^-$ increased the apparent Km value significantly with no change on the apparent Vmax value, suggesting a competitive inhibition on PAH uptake. And the inhibitory effect of $SCN^-$ on PAH uptake decreased with increase of pH in the incubation medium while that of isethionate increased with increase of pH. Intracellular water content, intracellular electrolyte concentration and oxygen consumption were not influenced by the replacement of $Cl^-$ with isethionate or $SCN^-$ in the incubation medium. These results suggest that both $isethionate^-$ and $SCN^-$ inhibit the PAH uptake by binding to some site necessary for normal PAH transport without affecting the cellular viability.

• The Korean Journal of Physiology and Pharmacology
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• 제3권1호
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• pp.93-100
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• 1999

The present study was designed to assess the roles of $PLA_2$ activation and arachidonic acid (AA) metabolites in hypoxia-induced renal cell injury. Hypoxia increased LDH release in a dose-dependent manner in rabbit renal cortical slices, and this increase was significant after 20-min hypoxia. The hypoxia-induced LDH release was prevented by amino acids, glycine and alanine, and extracellular acidosis (pH 6.0). Buffering intracellular $Ca^{2+}$ by a chelator, but not omission of $Ca^{2+}$ in the medium produced a significant reduction in hypoxia-induced LDH release. The effect of hypoxia was blocked by $PLA_2$ inhibitors, mepacrine, butacaine, and dibucaine. A similar effect was observed by a 85-kD $cPLA_2$ inhibitor $AACOCF_3.$ AA increased hypoxia-induced LDH release, and albumin, a fatty acid absorbent, prevented the LDH release, suggesting that free fatty acids are involved in hypoxia-induced cell injury. These results suggest that $PLA_2$ activation and its metabolic products play important roles in pathogenesis of hypoxia-induced cell injury in rabbit renal cortical slices.

• The Korean Journal of Physiology
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• 제2권1호
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• pp.59-71
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• 1968

The uptake of phenolsulfonphthalein (PSP) and of paraaminohippuric acid (PAH) by cortical slices of the rabbit kidney was investigated while varying the composition of medium. The overall uptake of these substances displayed typical active transport characteristics and was significantly enhanced in presence of acetate. When the phosphate buffer was used the optimal pH was 7.4 for both substances. However, when the tris-buffer was used the optimal pH was 7.4 for PSP and 8.3 for PAH. Removal of $Na^+$ from the medium resulted in a significant reduction in the uptake. Similar results, though lesser in magnitude, were obtained when either $K^+\;or\;Ca^{++}$ was removed from the medium. However, there was no additive effect when $K^+\;and/or\;Ca^{++}$ were additionally removed from the $Na^+-free$ medium. The presence of ${NH_4}^+$ greatly reduced while $Li^+\;and\;Mg^{++}$ moderately reduced the uptake of both substances. However, choline had no effect. In substrate-leached slices, acetate greatly enhance the uptake of organic acids; but this action was not demonstrable in absence of $Na^+,\;K^+\;or\;Ca^{++}$.

• 동국한의학연구소논문집
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• 제1권
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• pp.55-80
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• 1992

In order to examine that the effect of Sam Hwa San, circulating the vital energy of Sam Cho and controlling body fluid metabolism, gives any influence on renal function, changes in the urine flow, eletrolytes excretion, plasma aldosterone concentration and renin activity were observed after intravenous infusion of the Sam Hwa San extract in rabbit. Also in vitro effect of the herb extract on oxygen consumption in renal cortical slices and ATPase activity in kidney microsomes was measured. The following results were obtained : 1. The urine flow was markedly increased at 10 min after intravenous infusion of the Sam Hwa San extract($0.134{\pm}0.015$ vs. $0.433{\pm}0.046ml/min.kg$), but return ed to normal value after 40 min of infusion. 2. The glomerular filtration rate was significantly increased at 10 min after in travenous infusion of the Sam Hwa San extract, and the renal plasma flow at 10 and 20 min after infusion of the Sam Hwa San extract, following return to normal value. 3. $Na^+$ excretion was significantly increased during 10-40 min after intravenous infusion of the Sam Hwa San extract, although showed the maximal rate at 10-20 min. The fractional $Na^+$ excretion was also increased during 10-40 min. $K^+$ excretion was rapidly increased at 10 min after the intravenous Infusion of the Sam Hwa San extract and then gradually decreased to normal level at 40 min. The fractional $K^+$ excretion was significantly increased during 10-40 min after the intravenous infusion of the Sam Hwa San extract. 4. The plasma aldosterone concentration and renin activity were not altered by the infusion of the Sam Hwa San extract. 5. The ouabain-sensitive oxygen consumption of renal cortical slices was significantly reduced by the Sam Hwa San extract(0.5 and 1.0 vol.%). 6. The Na-K-ATPase activity of renal microsomes was strongly inhibited by the Sam Hwa San extract(0.5 and 1.0 vol.%). These results suggest that the Sam Hwa San causes a strong diuretic effect which results from reduction of Na reabsorption in renal tubule by a direct inhibition of Na-pump and, in part, from all increase in renal blood flow. In clinic, it is considered to obtain the therapeutic effect in body fluid metabolism disharmony to cause the circular disorder of vital energy.

• 대한한의학회지
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• 제21권3호
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• pp.119-128
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• 2000

목적 : Rhabdomyolysis에 의해 유발된 급성 신부전시 나타나는 신장세뇨관 세포에서 물질이동의 저해가 단삼 추출액에 의해 방지될 수 있는 지를 조사하였다. 방법 : 토끼에 50％ glycerol을 10ml/kg씩 대퇴근육내 주사한 후 뇨와 혈액을 채취하여 신기능을 측정하고, 신피질 절편을 분리하여 실험하였다. 결과： 토끼에 50％ glycerol을 10ml/kg씩 대퇴근육내 주사한 결과 사구체여과율의 감소와 Na 배설분율의 증가가 나타남으로서 glycerol 주입이 rhabdomyolysis에 의해 급성신부전이 유발되었음을 보였다. Glycerol을 주사하기 전 7일 동안 단삼 추출액 (0.05%)을 0.3 g/kg씩 경구 투여한 결과 glycerol에 의해 유발된 사구체여파율의 감소와 Na 배설분율의 증가가 유의하게 방지되었다. glycerol만을 주사한 동물에서는 포도당과 인산의 요배설분율이 각각 현저하게 증가하였으나, 이러한 증가는 단삼 추출액에 의해 억제되었다. 급성신부전이 유발된 신장피질에서 분리한 brush-border membrane vescicles (BBMV)에서 포도당과 인산의 이동은 정상 신장과 비교하여 유의한 감소가 나타나고, microsomal fraction에서 측정한 Na＋-K+-ATPase 활성도 억제되었다. 이러한 억제현상은 단삼 추출액을 전처치한 결과 방지되었다. 급성신부전이 유발된 신장피질 절편에서 유기 음이온인 P-aminohippurate 이동과 유기 양이온인 tetraethylammonium의 이동이 억제되었고, 이러한 변화는 단삼 추출액에 의해 방지되었다. Rhabdomyolysis에 의해 유발된 포도당과 인산의 배설분율의 증가는 항산화제로 잘 알려진 DPPD 전처치로 방지되었다. 결론 ： Rhabdomyolysis에 의한 급성신부전의 유발 과정에 반응성 산소기가 중요한 역할을 할 가능성을 보이고 있고, 단삼 추출액 전처치는 Rhabdomyolysis에 의한 급성 신부전시 나타나는 근위세뇨관에서 물질의 재흡수 장애를 방지하고 있다. 단삼 추출액의 방지 효과는 항산화작용에 기인할 것으로 사료된다.