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PubMed1984

Conceptual problems in establishing the critical concentration of cadmium in human kidney cortex.

The definition of the "critical concentration" for cadmium is compared with the concepts used to establish this measure in some recent publications. The term has not been clearly defined on a population basis and this has given rise to certain confusion. Different groups of investigators therefore have arrived at different estimates of the "critical concentration" for cadmium in human kidney cortex. A new measure, the "population critical concentration" (PCC) with a clearly defined response rate, is suggested. A reanalysis of the published data indicates that the PCC-10 (10% response rate) for cadmium in kidney cortex is likely to be in the range 180-220 micrograms/g and the PCC-50 is likely to be about 25% higher.

Cadmium Poisoning↗
PubMed1999

Kidney cortex cells derived from SV40 transgenic mice retain intrinsic properties of polarized proximal tubule cells.

BACKGROUND: We have developed a nontransformed immortalized mice kidney cortex epithelial cell (MKCC) culture from a mouse transgenic for a recombinant plasmid adeno-SV40 (PK4). Methods and Results. After 12 months in culture, the immortalized cells had a stable homogeneous epithelial-like phenotype, expressed simian virus 40 (SV40) T-antigen, but failed to induce tumors after injection in nude mice. Epithelium exhibited polarity with an apical domain bearing many microvilli separated from lateral domains by junctional complexes with ZO1 protein. The transepithelial resistance was low. A Na-dependent glucose uptake sensitive to phlorizin and a Na-dependent phosphate uptake sensitive to arsenate were present. Western blot analysis of membrane fractions showed that anti-Na-Pi antiserum reacted with a 87 kD protein. The Na/H antiporters NHE-1, NHE-2, and NHE-3 mRNAs were detected by reverse transcription-polymerase chain reaction (RT-PCR). The corresponding proteins with molecular weights of 111, 81, and 75 kD, respectively, could be detected by Western blot and were shown to be functional. Parathyroid hormone (PTH) induced a tenfold increase in cAMP and reduced the Na-dependent phosphate uptake and NHE-3 activity, as observed in proximal tubule cells. Isoforms alpha, delta, epsilon, and zeta of protein kinase C (PKC) were present in the cells. Angiotensin II (Ang II) elicited a translocation of the PKC-alpha toward the basolateral and apical domains. CONCLUSION: Thus, the MKCC culture retains the structural and functional properties of proximal tubular cells. To our knowledge, it is the first cell culture obtained from transgenic mice that exhibits the NHE-3 antiporter and type II Na-Pi cotransporter. MKCCs also display functional receptors for PTH and Ang II. Thus, MKCCs offer a powerful in vitro system to study the cellular mechanisms of ion transport regulation in proximal epithelium.

Angiotensin II↗
PubMedDate not supplied

[Energy metabolism in the kidney cortex of rats with alloxan diabetes].

Activity of lactate dehydrogenase was decreased in kidney cortex of rats with alloxane diabetes. The lactate dehydrogenase activity, catalyzing the lactate transformation into pyruvate, was increased. Activation of the pentosephosphate pathway enzymes was the characteristic property of metabolism impairments in kidney tissue under conditions of alloxane diabetes.

Animals↗
PubMed1994

Analysis of the Weinbaum-Jiji model of blood flow in the canine kidney cortex for self-heated thermistors.

The Weinbaum-Jiji equation can be applied to situations where: 1) the vascular anatomy is know; 2) the blood velocities are known; 3) the effective modeling volume includes many vessels; and 4) the vessel equilibration length is small compared to the actual length of the vessel. These criteria are satisfied in the situation where steady-state heated thermistors are placed in the kidney cortex. In this paper, the Weinbaum-Jiji bioheat equation is used to analyze the steady state response of four different sized self-heated thermistors in the canine kidney. This heat transfer model is developed based on actual physical measurements of the vasculature of the canine kidney cortex. In this model, parallel-structured interlobular arterioles and venules with a 60 microns diameter play the dominant role in the heat transfer due to blood flow. Continuous power is applied to the thermistor, and the instrument measures the resulting steady state temperature rise. If an accurate thermal model is available, perfusion can be calculated from these steady-state measurements. The finite element simulations correlate well in shape and amplitude with experimental results in the canine kidney. In addition, this paper shows that the Weinbaum-Jiji equation can not be used to model the transient response of the thermistor because the modeling volume does not include enough vessels and the vessel equilibration length is not small compared to the actual length of the vessel.

Animals↗
PubMed1980

Fate of glutamate carbon and nitrogen in isolated guinea-pig kidney-cortex tubules. Evidence for involvement of glutamate dehydrogenase in glutamine sythesis from glutamate.

1. The pathways and the fate of glutamate carbon and nitrogen were investigated in isolated guinea-pig kidney-cortex tubules. 2. At low glutamate concentration (1 mM), the glutamate carbon skeleton was either completely oxidized or converted into glutamine. At high glutamate concentration (5 mM), glucose, lactate and alanine were additional products of glutamate metabolism. 3. At neither concentration of glutamate was there accumulation of ammonia. 4. Nitrogen-balance calculations and the release of 14CO2 from L-[1-14C]glutamate (which gives an estimation of the flux of glutamate carbon skeleton through alpha-oxoglutarate dehydrogenase) clearly indicated that, despite the absence of ammonia accumulation, glutamate metabolism was initiated by the action of glutamate dehydrogenase and not by transamination reactions as suggested by Klahr, Schoolwerth & Bourgoignie [(1972) Am. J. Physiol. 222, 813-820] and Preuss [(1972) Am. J. Physiol. 222, 1395-1397]. Additional evidence for this was obtained by the use of (i) amino-oxyacetate, an inhibitor of transaminases, which did not decrease glutamate removal, or (ii) L-methionine DL-sulphoximine, an inhibitor of glutamine synthetase, which caused an accumulation of ammonia from glutamate. 5. Addition of NH4Cl plus glutamate caused an increase in both glutamate removal and glutamine synthesis, demonstrating that the supply of ammonia via glutamate dehydrogenase is the rate-limiting step in glutamine formation from glutamate. NH4Cl also inhibited the flux of glutamate through glutamate dehydrogenase and the formation of glucose, alanine and lactate. 6. The activities of enzymes possibly involved in the glutamate conversion into pyruvate were measured in guinea-pig renal cortex. 7. Renal arteriovenous-difference measurements revealed that in vivo the guinea-pig kidney adds glutamine and alanine to the circulating blood.

Aminooxyacetic Acid↗
PubMed2001

Galphas transcripts are biallelically expressed in the human kidney cortex: implications for pseudohypoparathyroidism type 1b.

Pseudohypoparathyroid type 1b patients are characterized by renal resistance to PTH in the absence of Albright's hereditary osteodystrophy or other endocrine abnormalities. Kindred studies have suggested that the cause of this resistance is a specific decrease in Galphas activity in renal proximal tubules due to paternal imprinting of Galphas. To test this, allelic expression of Galphas was analyzed in human fetal kidney cortex samples by RT-PCR assays. The results showed that, in contrast to the parent-specific expression of exon 1A and XLalphas (paternal) or NESP (maternal) mRNAs, Galphas transcripts are biallelically expressed in human kidney cortex. These data implicate abnormal imprinting of alternative regions within the GNAS1 locus as a more likely cause of pseudohypoparathyroid type 1b.

GTP-Binding Protein alpha Subunits, Gs↗
PubMed1994

Differentiation of kidney cortex peroxisomes in fetal and newborn rats.

Peroxisomal enzyme assays as well as cytochemical detection of catalase were carried out on fetal and newborn rat kidney cortex throughout the last 3 days of prenatal life and the first month of postnatal development. Concerning the patterns of peroxisomal enzymes, catalase activity, hardly detectable in the fetus, shows the strongest increment after the second week of postnatal life; beta-oxidation system and D-amino acid oxidase increase soon after birth; urate oxidase activity, detected in fetal life, rapidly decreases after birth; dihydroxyacetone phosphate-acyltransferase activity doubles at birth, remaining constant thereafter. Since by cytochemistry no catalase particles were detected in fetal kidneys, morphometric parameters were studied only postnatally. The numerical density shows only minor variations, mainly at day 3; the mean diameter remains practically unchanged between birth and day 14 but strongly increases later. The volume density pattern correlates in the early phase with the numerical density and later with the profile mean diameter. The results suggest that enzymes are asynchronously incorporated into pre-existing peroxisomes; that this import is faster in smaller organelles than in the larger, adult ones; that catalase increases after the H2O2-producing oxidases; and that the abrupt rise of beta-oxidation capacity and DH-APAT is related to the increased renal work immediately after birth.

Animals↗
PubMed1977

Homogeneous cell populations from rabbit kidney cortex. Proximal, distal tubule, and renin-active cell isolated by free-flow electrophoresis.

A single-cell suspension has been prepared from rabbit kidney cortex by using a Ca-binding medium and gentle mechanical forces. The suspension was subjected to carrier-free electrophoresis, and several cell fractions were obtained. Proximal and distal tubule cell populations could be identified by their morphology. Renin-containing cells were located by means of radioimmunoassay. The morphology of the cells and their vitality (uridine incorporation) are discussed.

Animals↗
PubMed1977

Purification and properties of human kidney-cortex hexosaminidases A and B.

Hexosaminidases (EC 3.2.1.30) A and B from human kidney cortex were purified to homogeneity by using concanavalin A affinity chromatography, ion-exchange chromatography and gel filtration. The yield of homogeneous isoenzymes improved approx. 20-fold, giving preparations of hexosaminidases A and B with specific activities of about 200 and 325 units/mg of protein respectively. The kinetic and structural properties of kidney hexosaminidase isoenzymes were studied and compared with the hexosaminidase isoenzymes from human placenta. The amino acid composition of hexosaminidase A was significantly different from that of hexosaminidase B. In the event of success in developing enzyme-replacement therapy for Tay-Sachs and Sandhoff's diseases, this modified procedure can furnish larger amounts of homogeneous isoenzymes.

Amino Acids↗
PubMed1996

Nonesterified fatty acid content of rabbit kidney cortex slices after warm ischemia and low temperature preservation.

Nonesterified fatty acid content (NEFA) of rabbit kidney cortex slices preserved at low temperature after warm ischemia was examined. Kidney tissue slices were subjected to 60 min of warm (37 degrees C) ischemia induced by anoxic gaseous phase incubation and then either had reperfusion simulated by normothermic oxygenated aqueous incubation or were preserved at 5 degrees C up to 18 h with UW sodium gluconate solution and then reincubated at normothermia. Slice NEFA content increased during ischemia and remained significantly higher than controls during simulated reperfusion. Ischemic tissue slice NEFA content was significantly reduced by both 3- and 18-h preservations. There was a significant increase in NEFA content in 3-h preserved slices during simulated reperfusion. This increase was relatively unaffected by the addition of KCN to the incubation medium, suggesting that mitochondrial injury was induced by ultrashort preservation of ischemic tissue slices. Ischemic tissue slices preserved for 18 h increased in NEFA content during simulated reperfusion but did not appear more damaged than slices subjected to ischemia alone. Addition of quinacrine (100 micromol/l) to the cold preservation solution significantly reduced NEFA content during simulated reperfusion of slices preserved both 3 and 18 h with a greater effect in 18-h preserved slices. Quinacrine had no effect when added only during simulated reperfusion. KCN addition during simulated reperfusion indicated that quinacrine acted as a mitochondrial protectant in the absence of phospholipase inhibition under these conditions. This study showed that cold preservation may be useful for resuscitation of ischemic tissues harvested for transplantation. Treatments administered during cold preservation of ischemic tissue can have a lasting beneficial effect during reperfusion and may be more effective than similar treatments given only during reperfusion.

Animals↗
PubMed1992

Regulation of glutamine metabolism in dog kidney cortex: effect of pH and chronic acidosis.

To examine the interrelationships of proton compartmentation and ammoniagenesis, experiments were performed in tubules and mitochondria isolated from dog kidney cortex. Tubules were incubated in Krebs-Henseleit buffer at different pH (pHe), and cytosolic pH (pHi) was estimated with the fluorescent probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Mitochondrial pH (pHm) was determined simultaneously in intact tubules by use of dimethyloxazolidine-2,4-dione. Over the pHe range 6.9-7.7, pHi was similar in control and acidotic dogs and linearly related to pHe. At pHe 7.4 in control tubules. pHm was 7.78 +/- 0.07, and varied little over the pHe range of 7.0-7.7. The pH gradient across the mitochondrial membrane rose at acid pHe. pHm was more alkaline when estimated in tubules from acidotic dogs compared with controls. Ammonium and glucose productions from glutamine were inversely related to pHe and pHi in tubules from both control and acidotic animals and were higher in acidosis. In contrast, ammonium production by isolated mitochondria did not vary as pHe was altered. Enzyme fluxes, calculated from metabolite changes, demonstrated that glutamate dehydrogenase (GDH) flux was altered. Enzyme fluxes, calculated from metabolite changes, demonstrated that glutamate dehydrogenase (GDH) flux was inversely and glutaminase (PDG) flux was linearly related to pHe. Ammonium production was significantly greater in mitochondria from acidotic dogs because of accelerated flux through PDG but not GDH. The present study demonstrates significant difference between proton compartmentation and regulation of ammoniagenesis in kidneys from acidotic dog compared with rat.

Acidosis↗
PubMed1978

Transport interaction phenomena between monoquaternary and polymethylene-bisquaternary amines in mouse kidney cortex slices.

The polymethylene-bisquaternary amine 14C-decamethonium accumulates in mouse kidney cortex slices incubated in Krebs-Ringer bicarbonate buffer (37 degrees C, pH 7.4) aerated with O2-CO2 95:5 v/v%. The accumulation rate was enhanced in the presence of monoquaternary amines which on the other hand depressed maximum accumulation ratio of decamethonium in the tissue. The stimulation phenomenon was apparently related to the intracellular concentration of monoquaternary amine since tissue preloaded with a monoquaternary amine took up decamethonium at an increased rate. This effect was due to an accelerated influx of decamethonium and not to inhibition of efflux since no decamethonium efflux was shown to occur in wash-out experiments. Flux stimulation may represent an interaction phenomenon of accelerative exchange diffusion type. Furthermore, various amines inhibited accumulation of decamethonium in a competitive manner. The study supports the idea that common steps are involved in cellular transport of monoquaternary and polymethylene-bisquaternary amines in the kidney.

Animals↗
PubMed1989

Isolation of myelin bodies from the kidney cortex of gentamicin-treated rats.

Myelin bodies have been isolated from the kidney cortex of gentamicin-treated rats (100 mg gentamicin sulfate/kg body weight i.p. twice daily for 3 days) by a simple procedure involving differential centrifugation followed by equilibrium density centrifugation on a discontinuous sucrose gradient. Electron microscopy and assay of acid phosphatase suggest that the myelin bodies were obtained in virtually quantitative yield, essentially uncontaminated by other cellular structures and relatively intact. The method developed here may also prove applicable for the isolation of myelin bodies arising in connection with other drug treatments and may provide information on a number of toxic side-effects of clinical importance.

Acid Phosphatase↗
PubMed1985

Purification, characterization, and activation of the glucocorticoid-receptor complex from rat kidney cortex.

The unactivated molybdate-stabilized glucocorticoid receptor (GcR) was purified from rat kidney cortex cytosol (RKcC) by using a modification of the procedure previously described by this laboratory for rat hepatic receptor. The purification includes affinity chromatography, gel filtration, and ion-exchange chromatography. The final preparation (approximately 1000-fold pure as determined from specific radioactivity) was used in subsequent physicochemical and functional analyses. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) showed a single heavily Coomassie-stained band at 90 kilodaltons. Density gradient ultracentrifugation indicated a sedimentation coefficient of 10.5 +/- 0.05 S (n = 2). Chromatography on an analytical gel filtration column produced a Stokes radius (Rs) of 6.4 +/- 0.07 nm (n = 5). The Rs was unchanged when the molybdate-stabilized GcR was analyzed in the presence of 400 mM KCl or when analyzed in the unpurified (cytosolic) state. In contrast, the hepatic GcR was observed to exist as a larger form in cytosol (7.7 +/- 0.2 nm). Following purification, or upon gel filtration analysis under hypertonic conditions, the Rs was similar to that of the unpurified RKcC GcR. Following removal of molybdate from RKcC GcR and thermal activation (25 degrees C/30 min), DNA-cellulose binding increased 1.5-2-fold over the unheated control. Addition of RKcC or hepatic cytosol (endogenous receptors thermally denatured at 90 degrees C/30 min or presaturated with 10(-7) M radioinert ligand) during thermal activation increased DNA-cellulose binding an additional 2-6-fold beyond the heated control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Diabetes-induced changes in glucose synthesis, intracellular glutathione status and hydroxyl free radical generation in rabbit kidney-cortex tubules.

Diabetes-induced changes in glucose formation, intracellular and mitochondrial glutathione redox states as well as hydroxyl free radicals (HFR) generation have been investigated in rabbit kidney-cortex tubules. In contrast to renal tubules of control animals, diabetes-evoked increase in glucose formation in the presence of either aspartate+glycerol+octanoate or malate as gluconeogenic precursors (for about 50%) was accompanied by a diminished intracellular glutathione reduced form (GSH)/glutathione oxidised one (GSSG) ratio by about 30-40%, while the mitochondrial GSH/GSSG ratio was not altered. However, a relationship between the rate of gluconeogenesis and the intracellular glutathione redox state was maintained in renal tubules of both control and diabetic rabbits, as concluded from measurements in the presence of various gluconeogenic precursors. Moreover, diabetes resulted in both elevation of the glutathione reductase activity in rabbit kidney-cortex and acceleration of renal HFR generation (by about 2-fold). On the addition of melatonin, the hormone exhibiting antioxidative properties, the control values of HFR production were restored, suggesting that this compound might be beneficial during diabetes therapy. In view of the data, it seems likely that diabetes-induced increase in HFR formation in renal tubules might be responsible for a diminished intracellular glutathione redox state despite elevated glutathione reductase activity and accelerated rate of gluconeogenesis, providing glucose-6-phosphate for NADPH generation via pentose phosphate pathway.

Animals↗
PubMed1990

Inhibition kinetics of cationic drugs on N'-methylnicotinamide uptake by brush border membrane vesicles from the dog kidney cortex.

The effect of cationic drugs on the uptake of the prototypical organic cation N'-methylnicotinamide has been evaluated. Using purified brush border membrane vesicles prepared from dog kidney cortex and applying a rapid Millipore filtration technique, cationic drugs apparent inhibitory constants (Ki) were calculated from kinetic analysis of N'-methylnicotinamide uptake corrected for noncarrier-mediated transport (10 s uptake; outwardly directed H+ gradient; pH 7.4, 25 degrees C). All of the cationic drugs tested exhibited competitive inhibition of N'-methylnicotinamide uptake suggesting that they all share the organic base transport system at the renal proximal tubule. The Ki values were as follows, in order of decreasing apparent affinity: quinidine (0.7 microM), trimehoprim (1.3 microM), cimetidine (2.0 microM), famotidine (3.0 microM), quinine (7.0 microM), amiloride (5.8 microM), procainamide (21 microM), and nizatidine (30 microM). The different relative affinities of the drugs for the organic base transport system may explain the mutual competition for renal tubular secretion observed when cationic drugs are administered concurrently in vivo, e.g., trimethoprim--procainamide and cimetidine--procainamide. The approach outlined in the present study should prove useful to predict complex drug interactions in clinical pharmacology.

Animals↗
PubMed1987

Changes in lysosome populations in the rat kidney cortex induced by passive Heymann glomerulonephritis.

Acute passive Heymann glomerulonephritis in rats induced heavy proteinuria and highly increased urinary activity of N-acetyl-beta-D-glucosaminidase, acid beta-galactosidase and acid phosphatase. The cortical activity of these acid hydrolases was increased essentially in the large lysosomes as demonstrated by subfractionation of the lysosome-rich mitochondrial-lysosomal fraction, by rate zonal centrifugation. Banding density of small lysosomes shifted or reduced to slightly lower value (1.225 g/ml), which is between the banding densities of small 'light' (1.20 g/ml) and small 'dense' lysosomes (1.235 g/ml) in normal rat kidney cortex. Labelled protein reabsorbed in the proximal tubule is recovered in these populations of small lysosomes as well as in the large lysosomes or 'protein droplets'. Glomerulonephritis also induced a new population of small 'light' lysosomes (density 1.185-1.195 g/ml) enriched in cathepsin D. The previously demonstrated morphological, biochemical, and physiological heterogeneity of renal lysosomes was confirmed and emphasized in the kidney cortex of glomerulonephritic rats. The main changes in the lysosomal populations appear to reflect the increased protein reabsorption as confirmed by the proteinuria.

Acetylglucosaminidase↗
PubMed1983

The effect of guanine nucleotides on [125I]-angiotensin binding in rat kidney cortex epithelial membranes.

Specific [125I]-angiotensin binding to crude basolateral/brush border membranes of rat kidney cortex was influenced by guanine nucleotides. The order of potency of nucleotides in their ability to decrease specific binding, was Gpp(NH)p greater than GTP greater than or equal to ITP greater than GDP greater than ATP greater than GMP greater than IDP. The kinetic alterations induced by a maximally effective concentration of Gpp(NH)p were: (a) a reduced steady state level of binding and (b) a markedly slower rate of ligand dissociation. The presence of Gpp(NH)p was found to increase the affinity of [125I]-angiotensin binding sites in rat renal cortex membranes. This contrasts with the decreases in affinity of [125I]-angiotensin binding reported in adrenal and mesenteric artery membranes.

Angiotensin II↗