[The isolated glomerulum of the ratkidney. III. Heterogeneity of lactate dehydrogenase in the kidney cortex, kidney medulla and glomerulum].
Explore the source record for details and available documents.
Humans↗
SEARCH · PubMed Health
Results for “Kidney Cortex”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Inhibitory effect of heminevrine on the metabolism of cerebral cortex, kidney cortex, liver and heart].
Explore the source record for details and available documents.
Animals↗
Effect of the aldose reductase inhibitor tolrestat on nerve conduction velocity, Na/K ATPase activity, and polyols in red blood cells, sciatic nerve, kidney cortex, and kidney medulla of diabetic rats.
Long-term prospective studies comparing the effects of conventional and intensive insulin therapy have linked diabetic hyperglycemia to the development of diabetic retinopathy, nephropathy, and neuropathy. The mechanisms through which glucose metabolism leads to the development of these secondary complications, however, are incompletely understood. In animal models of diabetic neuropathy, the loss of nerve function in myelinated nerve fibers has been related to a series of biochemical changes. Nerve glucose, which is in equilibrium with plasma glucose levels, rapidly increases during diabetic hyperglycemia because glucose entry is independent of insulin. This excess glucose is metabolized in large part by the polyol pathway. Increased flux through this pathway is accompanied by the depletion of myo-inositol, a loss of Na/K ATPase activity and the accumulation of sodium. Supportive evidence linking these biochemical changes to the loss of nerve function has come from studies in which aldose reductase inhibitors block polyol pathway activity, prevent the depletion of myo-inositol and the accumulation of sodium and preserve Na/K ATPase activity, as well as nerve function. The kidney and red blood cells (RBCs) are two additional sites of diabetic lesions that have been reported to develop biochemical changes similar to those in the nerve. We observed that polyol levels in the kidney cortex, medulla, and RBCs increased two- to ninefold in rats following 10 weeks of untreated diabetes. Polyol accumulation was accompanied by a 30% decrease in myo-inositol levels in the kidney cortex, but no change in RBCs or the kidney medulla. Na/K ATPase activity was decreased by 59% in RBCs but was unaffected in the kidney cortex or medulla. Aldose reductase inhibitor treatment that preserved myo-inositol levels, Na/K ATPase, and conduction velocity in the sciatic nerve also preserved Na/K ATPase activity in RBCs. Our results suggest that the pathophysiologic mechanisms underlying diabetic neuropathy are different from those of diabetic nephropathy. Our results also suggest that RBCs maybe a surrogate tissue for the assessment of diabetes-induced changes in nerve Na/K ATPase activity.
Aldehyde Reductase↗
[The biomorphosis of the kidney in swine. 2. Kidney cortex and kidney medulla].
Information recorded from structural development of kidney in swine foetuses of different age and in piglets together with functional data has shown that, notwithstanding progressing maturation, the capacity of renal corpuscles and tubules in piglets was less developed than in other species. Milk deficit or insufficient drinking water or medication may be considerable burdens on the kidney of newborn piglets and may cause stress-related damage.
Animals↗
Factors affecting human autopsy kidney-cortex and kidney-medulla platinum concentrations after cisplatin administration.
The objective of this study was to determine factors that affect cisplatin concentrations in human kidney cortex. We used flameless atomic absorption spectrophotometry to assay platinum in autopsy specimens of kidney cortex obtained from 83 cisplatin-treated patients. Concentrations were correlated with pretreatment factors and treatment conditions using univariate nonparametric statistics. Hierarchical stepwise multiple regression analyses of transformed (to normalize) data were then used to assess which factors were most important, controlling for other factors. Kidney-cortex platinum concentrations varied from 0 to 14.8 micrograms/g (median, 2.04 micrograms/g). The cumulative lifetime dose of cisplatin ranged from 10 to 1120 mg/m2 (median, 112 mg/m2). The time from the last cisplatin dose to death was < 1-609 days (median, 38 days). According to univariate statistics, factors that correlated (P < 0.05) with kidney-cortex platinum concentrations were the cisplatin dose per course, the pretreatment serum urea level, metoclopramide use (positive correlations), the time from the last cisplatin treatment to death, and the pretreatment serum albumin value (negative correlations). Factors that approached significance (0.05 < or = P < or = 0.10) were a history of hypertension, hyperbilirubinemia (positive), the serum calcium level, and phenytoin use (negative). In the multiple regression analysis, after controlling for the cisplatin dose per course and the time from the last treatment to death, only concurrent metoclopramide and phenytoin use entered the model. The hydration volume did not affect corrected kidney-cortex or kidney-medulla platinum concentrations. The following conclusions were reached: (1) it may be feasible to use lower hydration volumes than those used routinely, (2) any effect of hydration volume on cisplatin nephrotoxicity may not be mediated via a reduction in kidney-cortex platinum concentrations, (3) higher cisplatin doses might be tolerated with new 5-hydroxytryptamine-3 (5HT-3) antiemetics than were tolerated with metoclopramide, and (4) phenytoin should be tested for its ability to reduce cisplatin nephrotoxicity.
Autopsy↗
Properties of guanylate cyclase from rat kidney cortex and transplantable kidney tumors.
The subcellular distribution and properties of guanylate cyclase was examined in preparations of normal rat renal cortex and Morris renal tumors MK2 and MK3. In normal kidney cortex about two-thirds of guanylate cyclase activity of homogenates was found in soluble fractions. With renal tumors the homogenate activity was less and the enzyme was equally divided between particulate and soluble fractions. The particulate enzyme in kidney cortex and tumors was associated with all particulate fractions. Triton X-100 increased the activity of all preparations. All preparations preferred Mn2+ as the sole cation. The stimulatory effects of Ca2+ on soluble enzyme and inhibitory effects on particulate activity were similar with preparations of renal cortex and tumors. ATP inhibited all preparations. Soluble and particulate guanylate cyclases from renal cortex were activated several-fold with 1 mM NaN3. Preparations of tumor enzymes did not respond to NaN3. Thus, compared to normal renal cortex the subcellular distribution of guanylate cyclase and some of its properties are altered in preparations of renal tumors.
Animals↗
Cadmium in kidney cortex, liver, and pancreas from Swedish autopsies. Estimation of biological half time in kidney cortex, considering calorie intake and smoking habits.
Cadmium and zinc have been analyzed in tissues from 292 persons autopsied in Stockholm. In kidney cortex, liver, and pancreas the individual cadmium levels are distributed in a lognormal way. In kidney cortex there is a continuous accumulation of cadmium with age up to 50 years, followed by a decrease. Smokers show a higher cadmium accumulation. For nonsmokers, the biological half time of cadmium in kidney cortex is estimated at 30 years, with an average concentration at age 50 of 11 mug/g wet weight. When smokers are included, the average cadmium concentration at age 50 is 22 mug/g wet weight. Based on the more pronounced cadmium accumulation among smokers than nonsmokers, the respiratory absorption rate of cadmium from tobacco smoke is estimated to be approximately 50%.
Adolescent↗
[Changes in the activity and inductibility of O-demethylase in kidney cortex and liver following kidney damage induced by Salyrgan (author's transl)].
Explore the source record for details and available documents.
Animals↗
Purification and partial characterization of a thiol proteinase activating prokallikrein from the rat kidney cortex.
The rat kidney cortex contains at least three kinds of prokallikrein-activating proteinase, and among these the one with the highest molecular weight was purified by a procedure including chromatography on CM-cellulose, concanavalin A-Sepharose, organomercurial-Sepharose 4B and Sephadex G-100. The resulting preparation was apparently homogeneous, as assessed by SDS-polyacrylamide gel electrophoresis. The molecular weight was estimated to be 57,000. The optimal pH for the activation of prokallikrein by the preparation, termed activator I, was around 4.5. Activator I was inhibited by E-64, iodoacetate and leupeptin, but not by PMSF and phosphoramidon. In immunodiffusion analysis, the antiserum to activator I formed an immunoprecipitin arc with the extract from the kidney cortex or submandibular gland, but not with that from the pancreas. These results indicate that activator I is a thiol proteinase with a molecular weight of 57,000. A proteinase immunologically identical with activator I appears to be present in the submandibular gland.
Amino Acids↗
Utilization of alanine for glucose formation in isolated rabbit kidney-cortex tubules.
In kidney cortex tubules isolated from fed rabbits L-alanine is not utilized as glucose precursor, when added as a sole substrate. However, this amino acid decreases gluconeogenesis from low (up to 1 mM) 2-oxoglutarate concentrations and stimulates this process at higher (2.5-10 mM) ketoacid contents in the suspension medium. Aminooxyacetate, an inhibitor of aminotransferases, abolishes both inhibitory and stimulatory effects of L-alanine on glucose formation. The addition of 2-oxoglutarate increases the incorporation of L-[U-14C]alanine to glucose from 8- to 123-fold, depending upon the ketoacid and alanine concentrations used. In contrast, nonlabelled L-alanine decreases the incorporation of low [U-14C)2-oxoglutarate concentrations into glucose, while it does not affect contribution of 5 mM ketoacid to gluconeogenesis. The data indicate that (i) in the presence of 2-oxoglutarate L-alanine is utilized as glucose precursor in rabbit renal tubules and (ii) this amino acid may decrease the contribution of low extracellular concentrations of the ketoacid to gluconeogenesis.
Alanine↗
Antagonism between parathyroid hormone and norepinephrine on cyclic adenosine-3':5'-monophosphate (cAMP) levels in isolated tubules from rat kidney cortex.
Isolated rat kidney cortex tubules were used as a model system to study the hormonal regulation of cyclic adenosine-3':5'-monophosphate (cAMP) levels in vitro. When incubated over 15 min, parathyroid hormone increased cAMP levels 4-fold in the absence of inhibitors of cAMP phosphodiesterase. Norepinephrine in a concentration of 5-10-7 M which had itself no effect on cAMP levels under this condition, inhibited the effect of parathyroid hormone by 50%. This effect of the catecholamines could be completely abolished by the addition of an alpha-receptor blocking agent, phentolamine. The addition of an inhibitor of cAMP phosphodiesterase, in a concentration sufficient to prevent the breakdown of extratubular cAMP, potentiated hormone effects on cAMP levels. The antagonism between catecholamines and parathyroid hormone on cAMP levels was however not abolished by this treatment. This indicated that catecholamines probably inhibited parathyroid hormone stimulated cAMP formation. Since most of the cAMP was found to be intratubular, it can be assumed that norepinephrine and parathyroid hormone interact in the same cell. Proximal tubular sodium reabsorption and renal gluconeogenesis are discussed as possible events of this hormone interaction.
Animals↗
Effect of osmotic shocks on rabbit kidney cortex slices.
Rabbit kidney cortex slices behave an osmometers when withstanding hyperosmotic or hyposmotic shocks of amplitude up to pi 1/pi 2 = 1.25. For hyposmotic shocks of amplitude larger than or equal to pi 1/pi 2 = 1.50, the maximum swelling achieved is less than what can be expected on the basis of the van't Hoff relation, thereby indicating that a volume regulation process is taking place. Volume regulation in kidney slices can be dissociated into two distinct phases. The first one, of swelling limitation, is very rapid and keeps maximum cell volume at values lower than expected when the tissue is considered as an osmometer. This phase is followed by a slow volume readjustment process during which volume progressively decreases towards control values. The major intracellular osmotic effector loss during both swelling limitation and volume readjustment is Na+. The overall volume regulation process is insensitive to furosemide, vanadate, and bumetanide. Swelling limitation is blocked by addition of ouabain. Contrary to what has been believed previously, there is, however, no need to implicate control of the activity of a ouabain-sensitive, Na+/K+ pump in the Na-dependent volume regulation mechanism.
Amino Acids↗
Creatine transport in brush-border membrane vesicles isolated from rat kidney cortex.
The kidney efficiently salvages creatine from the urine; however, the mechanism(s) that mediates renal creatine reabsorption has not been investigated. This study characterizes the creatine transport mechanism in brush-border membrane vesicles isolated from the rat renal cortex. An osmolality plot revealed that creatine is transported into an osmotically active space and that it is also bound to the membranes. An inwardly directed NaCl gradient stimulated creatine uptake and the time course of uptake exhibited an overshoot phenomenon, which indicates the presence of an active process for creatine in these membranes. The uptake of creatine showed an absolute requirement for both Na(+) and Cl(-). The NaCl gradient-dependent creatine uptake was stimulated by a valinomycin-induced, inside-negative, K(+)-diffusion potential, which suggests that the uptake process is electrogenic. Stoichiometric analyses indicated a probable couple ratio of 2 Na(+):1 Cl(-):1 creatine molecule. The kinetic study showed that creatine is transported by a high-affinity system (K(m) of 15 microM). Creatine uptake was inhibited by a 100-fold excess of various compounds with the following potency order: cold creatine = guanidinopropionic acid > nipecotic acid > gamma-aminobutyric acid (GABA) = beta-alanine = betaine, whereas carnitine, glycine, taurine, and choline were without effect. This pattern of inhibition differs from that observed for GABA uptake (unlabeled GABA = GPA > beta-alanine > nipecotic acid >> creatine). The conclusion drawn was that the apical membrane of the renal cortical tubules contains an active, high-affinity, electrogenic, 2 Na(+)/1 Cl(-)/creatine cotransporter.
Animals↗
Cadmium/zinc relationships in kidney cortex and metallothionein of horse and red deer: histopathological observations on horse kidneys.
Cadmium and zinc were determined in kidney cortex of 63 horses and 51 red deer (Cervus elaphus). Cadmium and zinc were also determined in protein fractions obtained by Sephadex chromatography of kidney cortex from 10 horses and 4 red deer. Histopathological parameters in kidney cortex of horses were compared to cadmium content. The metal contents (on wet weight basis) in kidney cortex of the horses were 0.31 +/- 0.22 mmole Cd/kg (range 0.03-1.21) and 0.63 +/- 0.17 mmole Zn/kg (range 0.36-1.23). The Zn content increased with the Cd content, the Zn increase being less at higher concentrations. No significant increase of the Cd content with age of the horses (range 2-19 years) was found. The metal contents in kidney cortex of the red deer were 0.030 +/- 0.031 mmole Cd/kg (range 0.002-0.13) and 0.51 +/- 0.37 mmole Zn/kg (range 0.30-2.82). Here the Zn content did not increase significantly with Cd content, and in this case a positive linear relation of Cd content with age of the deer (range 0-11 years) was observed. The molar Zn/Cd ratio in the metallothionein fractions of horse kidney cortex was less variable at higher Cd contents. All Cd and the increase of Zn above an average basal level of 0.36 mmole Zn/kg was recovered in the metallothionein fractions. No gross histopathological changes could be observed in kidney cortex of the horses. Nevertheless a slight increase of the thickness of the basement membrane of Bowman's Capsule and also of the diameter of Bowman's Capsule in relation to Cd content up to 0.3 mmole/kg could be observed.
Animals↗
Identification of an external NADH oxidase in rat kidney cortex mitochondria.
Intact rat kidney cortex mitochondria oxidize external NADH and NADPH. Basal NADH oxidation of mitochondria, but not basal NADPH oxidation, is stimulated by hexammine-ruthenium (HR). 10.7 mumol/l HR induce 50% of the maximal NADH-oxidizing activity and amounted to 169 nmol NADH/min/mg of mitochondrial protein. The HR-stimulated NADH oxidation involves a stoichiometric 1:1 oxygen consumption. The electron transfer from NADH to oxygen does not occur via the respiratory chain complex I, but is connected with a superoxide anion radical formation. Experiments with intact mitochondria, submitochondrial particles and inner mitochondrial membranes show that rat kidney cortex mitochondria possess a NADH oxidase localized on the outer surface of the inner mitochondrial membrane.
Animals↗
Effect of bicarbonate on glutamine and glutamate metabolism by rat kidney cortex mitochondria.
Isolated rat kidney cortex mitochondria were incubated at pH 7.4 in the presence or absence of a CO2/bicarbonate buffer (28 mM) to investigate the pH-independent role of bicarbonate on glutamine and glutamate metabolism. Changes in the concentration of key intermediates and products during the incubations were used to calculate metabolite flux rates through specific mitochondrial enzymes. With 1 mM glutamine and 2 mM glutamate as substrates, bicarbonate caused an inhibition of glutamate oxalacetate transaminase flux and a stimulation of glutamate deamination. The same effects were also produced with addition of either aminooxyacetate or malonate. These effects of bicarbonate were prevented when 0.2 mM malate was included as an additional substrate. Bicarbonate ion was identified as a potent competitive inhibitor of rat kidney cortex succinate dehydrogenase. These results indicate that aminooxyacetate, malonate, and bicarbonate all act to stimulate glutamate deamination through a suppression of glutamate transamination, and that the control by transamination of glutamate deamination is due to alterations in alpha-ketoglutarate metabolism. In contrast, in mitochondria incubated with glutamine in the absence of glutamate, bicarbonate was found to inhibit glutamate dehydrogenase flux. This effect was found to be due in part to the lower intramitochondrial pH observed in incubations with bicarbonate. These findings indicate that bicarbonate ion, independent of pH, may have an important regulatory role in renal glutamine and glutamate metabolism.
Aminooxyacetic Acid↗
[Activation characteristics of ouabain-sensitive respiration and Na,K-ATPase in the kidney cortex and medullary zone of rats adapted to cold].
The endogenous and ouabain-sensitive respiration and Na, K-ATPase activity in the cortex and kidneys medulla of the cold-acclimated male albino rats have been determined. The increase of the respiration rate has been stated to be caused by the Na-pump activation. The obtained changes of Na, K-ATPase activity are supposed to be connected with the regulation of concentration and sodium excretion function of kidneys.
Adaptation, Physiological↗
Tolerance to osmotic shocks in rats kidney cortex and medulla.
Kidney medulla cells of mammals have to cope with large changes in environmental osmolarity, a challenge most other mammalian cells never have to experience. In these last cells, application of osmotic shocks induces dramatic modifications in chromatin organization. The present paper reports on the changes of medulla cell chromatin in situ, in rat kidney slices submitted to osmotic challenges and in vitro, on preparations of extracted chromatin submitted to changes in environmental ion concentrations. Our results show that the chromatin of kidney medulla cells: (1) does not behave differently from the other mammalian chromatins when submitted in situ or in vitro to osmotic challenges; (2) presents in vitro physico-chemical characteristics similar to those of the other mammalian chromatins; and (3) is protected in vitro, as the other mammalian chromatins, from the disrupting effects of increases in inorganic ion concentrations by different compensatory organic solutes. The ability of kidney medulla cells to adapt to large increases in osmolarity could thus be related to a rapid control of the level of such compounds rather than to some rather specific, intrinsic molecular adaptations of macromolecules.
Animals↗