• 제목/요약/키워드: Reabsorption

검색결과 185건 처리시간 0.019초

Effect of Diet and Water Intake on Aquaporin 2 Function

  • Kim, Jun-Mo;Kim, Tae-Hee;Wang, Tong
    • Childhood Kidney Diseases
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    • 제20권1호
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    • pp.11-17
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    • 2016
  • Appropriate control of diet and water intake is important for maintaining normal blood pressure, fluid and electrolyte homeostasis in the body. It is relatively understood that the amount of sodium and potassium intake directly affects blood pressure and regulates ion transporters; Na and K channel functions in the kidney. However, little is known about whether diet and water intake regulates Aquaporin (AQP) function. AQPs, a family of aquaporin proteins with different types being expressed in different tissues, are important for water absorption by the cell. Water reabsorption is a passive process driven by osmotic gradient and water permeability is critical for this process. In most of the nephron, however, water reabsorption is unregulated and coupled to solute reabsorption, such as AQP1 mediated water absorption in the proximal tubule. AQP2 is the only water channel founded so far that can be regulated by hormones in the kidney. AQP2 expressed in the apical membrane of the principal cells in the collecting tubule can be regulated by vasopressin (antidiuretic hormone) controlling the final volume of urine excretion. When vasopressin binds to its receptor on the collecting duct cells, it stimulates the translocation of AQP2 to the membrane, leading to increased water absorption via this AQP2 water channel. However, some studies also indicated that the AQP2 is also been regulated by vasopressin independent mechanism. This review is focused on the regulation of AQP2 by diet and the amount of water intake on salt and water homeostasis.

A Study on $Na^+$ and Water Reabsorption in the Nephron Segment Beyond Proximal Tubule Measured by Lithium Clearance

  • Han, O-Soo;Goo, Yong-Sook;Sung, Ho-Kyung
    • The Korean Journal of Physiology
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    • 제25권2호
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    • pp.189-200
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    • 1991
  • During the past few years it has been proposed that lithium clearance can be used as a reliable measure for the outflow of tubular fluid from the proximal tubule. This study was aimed to characterize the inflow dependent reabsorption of Na in renal tubule beyond the proximal tubule. For this purpose, lithium clearance was used as a measure for the inflow from the proximal tubule and the changes in reabsorption fraction of Na and water were determined in rabbits. Rabbits were pretreated with hypotonic saline solutions for an hour (50 mM/L NaCl, 20 ml/hr/kg). And then a hypertonic solution of 500 mM/L NaCl (20 ml/kg) was administered intraperitoneally in conjunction with a bolus of LiCl solution (2 mM/kg, i.v.) for conditioning the $C_{Li}$ and urine flow rate. To rule out the effect of $Li^+$ on tubular functions, a bolus of NaCl solution (2 mM/kg, i.v.) was administered. Fifteen, thirty, and sixty minutes after injection of hypertonic saline arterial blood and urine samples were taken. Urinary and plasma concentrations as well as urinary output of $Li^+,\;Na^+\;and\;K^+$ were measured. From these $C_{Li},\;C_{Na}$ and the reabsorption fraction of Na and water $(Fr_{Na}\;&\;FrH_2O)$ were calculated. These results were compared with those from control groups in which the same amount of isotonic saline (145 mM/L NaCl) and of 15% dextran solution were administered in the same way as that in experimental group. Followings are the results obtained. 1) The plasma concentration of $Na^+$ in rabbits injected with hypertonic saline reached the peak value after 15 min and thereafter no significant change was observed. Hematocrit values did not show any change, while urinary excretion of $Na^+$ increased markedly during the first 15 min and decreased thereafter. These results were not affected by an injection of a small amount of LiCl. 2) The clearances of $Li^+,\;Na^+\;and\;K^+$ in rabbits injected with hypertonic saline and LiCl solution decreased. 3) In spite of the variation in $C_{Li},\;Fr_{Na}$ did not show any significant change while $FrH_2O$ increased gradually. 4) $C_{Li}$ decreased also in rabbits received isotonic saline. $Fr_{Na}$ tended to be higher than that in hypertonic saline group, while $FrH_2O\;and\;Fr_{Na}$ did not associated with the decrease in $C_{Li}$. 5) $C_{Li}$ of the rabbits received dextran solution fluctuated persistently and $Fr_{Na}\;and\;FrH_2O$ did not change in along with $C_{Li}$ although $Fr_{Na}$ had a tendency to be higher than that in hypertonic saline group. 6) From the above results it was concluded that: (a) In rabbits with normal body store of $Na^+$, the $Fr_{Na}$ of renal tubule beyond proximal tubule. calculated from $C_{Li}$ as a measure of inflow from proximal tubule is constant in spite of variations in $C_{Li}$. (b) The $FrH_2O$ calculated from $C_{Li}$ is dependent largely upon ADH rather than inflow from proximal tubule. (c) When there is a decrease in plasma $Na^+$ concentration or ineffective body fluid. $Li^+$ reabsorption may occur in the thick segnent of Henle's loop and hence the determination of $Fr_{Na}$ and $FrH_2O$ will not be easy one, but $Fr_{Na}$ is constant under the same experimental conditions.

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METABOLIC ACIDOSIS INFLUENCES ON RENAL SODIUM HANDLING IN CADMIUM-INTOXICATED RATS

  • Kim, Yung-Kyu
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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    • pp.107-107
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    • 2002
  • It has been reported that antinatriuresis is induced by acute cadmium intoxication. However, the mechanisms related to the increase in renal sodium reabsorption by cadmium exposure is not clear yet although it has been suggested that the elevated aldosterone might involve in this process.(omitted)

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측뇌실내(側腦室內) Nalprphine의 가토신장기능(家兎腎臟機能)에 미치는 영향(影響) (Influence of Intracerebroventricular Nalorphine on the Renal Function of the Rabbit)

  • 국영종;최봉규;김흥규
    • 대한약리학회지
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    • 제16권2호
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    • pp.1-7
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    • 1980
  • As it has been reported that morphine induce antidiuresis, and antinatriuresis along with decrease in renal hemodynamics when given intracerebroventricularly[ivt], the renal action of nalorphine, a partial antagonist of morphine action, and its influence upon the morphine action were investigated in this study. $10{\mu}g/kg$ of nalorphine given into the lateral ventricle of the rabbit brain tended to decrease renal plasma flow and glomerular filtration rate and increase the reabsorption of free water in the tubules. $100{\mu}g/kg$ ivt significantly decreased urine flow rate and increased free water reabsorption, and tended to increase electrolyte excretion in spite of decrease in renal plasma flow and glomerular filtration, suggesting that ADH also involved in the antidiuresis. Morphine hydrochloride, $10{\mu}g/kg$, ivt, produced marked decrement in renal hemodynamics along with decreased excretions of sodium, potassium and water, and these morphine actions were alleviated by nalorphine given 20 min later. The natriuretic action of ivt nalorphine manifested itself uninfluenced by the morphine. These observations indicate that nalorphine ivt produces renal actions similar to those of morphine, though less potent, and that it can antagonize the latter action. It is suggested that morphine influences renal hemodynamics through nerve by stimulating the 'morphine receptor' in the brain, whereas nalorphine liberates ADH by the agonistic action on the 'nalorphine receptor'.

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백색 LED 패키지용 형광체 광학 시뮬레이션 정확도에 관한 연구 (Accuracy-Enhancement of Optical Simulation for a White LED Based on Phosphors)

  • 노주현;전시욱;김재필;송상빈;여인선
    • 조명전기설비학회논문지
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    • 제29권6호
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    • pp.27-34
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    • 2015
  • There has been a critical issue in optical simulation of phosphors in LEDs due to their light-reabsorption properties. To improve the accuracy of optical modeling for a white LED package, we utilized the spectrum data of the phosphor-dispersed encapsulant film instead of the phosphor powder. By measuring white LED packages with green and red phosphors, the maximum difference between simulation and experimental results of a color temperature, a color rendition index number and a color coordinate corresponds to ${\Delta}T=95K$, ${\Delta}Ra=1.7$ and ${\Delta}xy=0.007$, respectively. Based on those results, the proposed method can well explain the change of emission spectra of white LEDs with more than two phosphors which introduce the complex optical phenomena such as absorption, reabsorption, light emission, reflection and scattering, etc.

Verapamil이 개의 신장기능에 미치는 영향 (Effect of Verapamil on Renal Function in Dog)

  • 고석태;허영근
    • 약학회지
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    • 제35권2호
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    • pp.85-98
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    • 1991
  • Verapamil, $Ca^{2+}$-channel blocker, when given into vein or into carotid artery, produced the decrease of urine flow accompanied with the decreased amounts of Na$^{+}$ and $K^{+}$ excreted in urine ($E_{Na}, E_{K}$) and with the decreased clearances of free water (C$_{H_2O}$) and osmolar substance (C$_{osm}$), and then increased reabsorption of Na$^{+}$ and $K^{+}$ in renal tubules (R$_{Na}$, R$_{N}$), glomeruler filtration rate (GFR) and renal plasma flow (RPF) were inhibited when verapamil was given into carotid artery, but were only tendency of reduction when given intravenously. Verapamil, when infused into a renal artery, exhibited diuresis accompanied with the increased GER, RPF, E$_{Na}$ and E$_{K}$, with the decreased filtration fraction (FF) in only infused kidney. At the same time, $C_{H_2O}$ was not changed, R$_{Na}$ and R$_{K}$ were reduced. Antidiuretic action by verapamil administered into vein or into carotid artery in normal kidney was reversed to diuretic action in denervated kidney. At this time, parameters of renal function exhibited the opposite phenomena compared to that elicited by verapamil in normal kidney, wherease renal denervation did not influence the action of verapamil infused into a renal artery. Above results suggest that verapamil produce both antidiuresis through nervous system centrally, not endogenous substances and diuresis by direct action in the kidney. Diurectic action are caused by hemodynamic improvement through dilatioon of vas efferense and by greatly inhibited reabsorption of electrolytes in distal tubules.

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Dopamine $D_1$ Receptor 효능제인 SKF 81297의 신장작용 (Renal Action of SKF 81297, Dopamine $D_1$ Receptor Agonist, in Dogs)

  • 고석태;정경희
    • Biomolecules & Therapeutics
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    • 제9권3호
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    • pp.209-217
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    • 2001
  • This study was attempted to investigate on renal effect of ($\pm$)6-chloro-7,8-dihydroxy-1-phenol 2,3,4,5-tetrahydro-lH-3 benzazepine (SKF 81297), dopamine $D_1$ receptor agonist, in dog. SKF 81297, when gluten intravenously, produced diuretic action along with the increases of renal plasma flow (RPF), glomerular filtration rate (GFR), amounts of N $a^{+}$ and $K^{+}$ excreted into urine ( $E_{Na}$ , $E_{K}$) and osmolar clearance ( $C_{osm}$). It also decreased the reabsorption rates of N $a^{+}$ and $K^{+}$ in renal tubule ( $R_{Na}$ , $R_{K}$) and free water clearance ( $C_{H2O}$), whereas ratios of $K^{+}$ agonist N $a^{+}$ in urine and filtration fraction (FF) was not changed. SKF 81297, when administered into a renal artery, elicited diuresis both in experimental kidney given the SKF 81297 and control kidney not given, while the effect was more remarkable in experimental kidney than those exhibited in control kidney. SKF 81297 given into carotid artery also exhibited diuresis, the potency at this time, compared to those induced by intravenous SKF 81297, was magnusgreat. Above results suggest that SKF 81297 produces diuresis by both indirect action through changes of central function and direct action being induced in kidney. Central diuretic action is mediated by improvement of renal hemodynamics, but direct action by inhibition of electrolytes reabsorption in renal tubule.enal tubule. tubule.

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$K^+$ Channel 개방제인 BRL 34915의 신장작용 (Renal Action of BRL 34915, a $K^+$ Channel Opener, in Dog)

  • 고석태;최홍석
    • 약학회지
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    • 제44권3호
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    • pp.205-212
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    • 2000
  • The effect of BRL 34915, a $K^{+}$ channe$Na^{+}$l opener, on renal function was investigated in anesthetized dog. BRL 34915, when given into the vein, elicited the decrease of urine volume accompanied with the reduction of renal plasma flow (RPF), osmolar clearance ($C_{osm}$) and amounts of sodium excreted into urine ($E_{na}$), whereas reabsorption rate of sodium in renal tubules ($R_{na}$), ratio of $K^{+}$ against $Na^{+}$ in urine ($K^{+}$ /$Na^{+}$) were elevated significantly with a partial fall of mean arterial pressure (MAP). BRL 34915 injected into a renal artery produced the diuretic action along with the increase in RPF $C_{osm}$, $E_{na}$ and amounts of potassium excreted in urine ($E_{k}$), and the decrease in $R_{na}$, reabsorption rate of potassium in renal tubules ($R_{k}$), free water clearance ($C_{H20}$) and $K^{+}/Na^{+}$ ratio in only ipsilateral kidney, however changes of the renal function were not observed in control kidney. BRL 34915 given into carotid artery exhibited the same aspect as changes of renal function induced by intravenous BRL 34915. These results suggest that BRL 34915 has dual effects, renally acting diuretic and centrally acting antidiuretic action.n.

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Estimation of the Endogenous Pancreatic/Biliary Zinc Pool and the Effect of Phytate and Calcium on Zinc Homeostasis

  • Kwun, In-Sook;Donald Oberleas
    • Preventive Nutrition and Food Science
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    • 제2권1호
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    • pp.35-41
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    • 1997
  • The pancreas is an important organ in the maintenance of zinc homeostasis. Endogenous zinc is con-tinuously secreted via pancreatic exocrine fluid or to a lesser extent in bile. Much of the endogenous secretion must be reabsorbed to sustain zinc homeostasis. The objective of this study was to estimate the relative size of the pancreatic/biliary zinc pool in comparision to the dietary zinc intake, and to study the effect of the phytate and calcium on the zinc homeostasis using a rat model. At the termination of the experiment, pan-creatic/biliary fluid was collected from the rats. Both radioactivity and total zinc were measured and the relative size of the pancreatic/biliary zinc pool was estimated. To determine the effect of phytate and calcium on zinc homeostsis, dietary zinc intake, the amount of zinc in pancreatic.biliary fluid and fecal zinc excretion were measured. The flow rate of pancreatic/biliary fluid, as corrected for tubing constriction, gives the corrected zinc concentration in the pancreatic/biliary fluid was 2.2 times higher than dietary zinc intake. To maintain zinc homeostasis, zinc absorption/reabsorption was very efficient in the current model; 76%, 88% of absorption/reabsorption for low calcium group and high calcium group 81% for phytate group and non-phytate group, respectively.

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Changes in Renal Brush-Border Sodium-Dependent Transport Systems in Gentamicin-Treated Rats

  • Suhl, Soong-Yong;Ahn, Do-Whan;Kim, Kyoung-Ryong;Kim, Jee-Yeun;Park, Yang-Saeng
    • The Korean Journal of Physiology and Pharmacology
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    • 제1권4호
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    • pp.403-411
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    • 1997
  • To elucidate the mechanism of gentamicin induced renal dysfunction, renal functions and activities of various proximal tubular transport systems were studied in gentamicin-treated rats (Fisher 344). Gentamicin nephrotoxicity was induced by injecting gentamicin sulfate subcutaneously at a dose of 100 $mg/kg{\cdot}day$ for 7 days. The gentamicin injection resulted in a marked polyuria, hyposthenuria, proteinuria, glycosuria, aminoaciduria, phosphaturia, natriuresis, and kaliuresis, characteristics of aminoglycoside nephropathy. Such renal functional changes occurred in the face of reduced GFR, thus tubular transport functions appeared to be impaired. The polyuria and hyposthenuria were partly associated with a mild osmotic diuresis, but mostly attributed to a reduction in free water reabsorption. In renal cortical brush-border membrane vesicles isolated from gentamicin-treated rats, the $Na^+$ gradient dependent transport of glucose, alanine, phosphate and succinate was significantly attenuated with no changes in $Na^+-independent$ transport and the membrane permeability to $Na^+$. These results indicate that gentamicin treatment induces a defect in free water reabsorption in the distal nephron and impairs various $Na^+-cotransport$ systems in the proximal tubular brush-border membranes, leading to polyuria, hyposthenuria, and increased urinary excretion of $Na^+$ and other solutes.

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