Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Kidney Cortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,225 records · Page 68Linked to original sources
PubMed1986

Plasma membrane proton ATPase from human kidney.

Distal urinary acidification is thought to be mediated by a proton ATPase (H+-ATPase). We isolated a plasma membrane fraction from human kidney cortex and medulla which contained H+-ATPase activity. In both the cortex and medulla the plasma membrane fraction was enriched in alkaline phosphatase, maltase, Na+,K+-ATPase and devoid of mitochondrial and lysosomal contamination. In the presence of oligomycin (to inhibit mitochondrial ATPase) in the presence of ouabain (to inhibit Na+,K+-ATPase) and in the absence of Ca (to inhibit Ca2+-ATPase) this plasma membrane fraction showed ATPase activity which was sensitive to dicyclohexylcarbodiimide and N-ethylmaleimide. This ATPase activity was also inhibited by vanadate, 4,4'-diisothiocyano-2,2'-disulfonic stilbene and ZnSO4. In the presence of ATP, but not GTP or UTP, the plasma membrane fraction of both cortex and medulla was capable of quenching of acridine orange fluorescence, which could be dissipated by nigericin indicating acidification of the interior of the vesicles. The acidification was not affected by presence of oligomycin or ouabain indicating that it was not due to mitochondrial ATPase or Na+,K+-ATPase, respectively. Dicyclohexylcarbodiimide and N-ethylmaleimide completely abolished the acidification by this plasma membrane fraction. In the presence of valinomycin and an outward-directed K gradient, there was increased quenching of acridine orange, indicating that the H+-ATPase is electrogenic. Acidification was not altered by replacement of Na by K, but was critically dependent on the presence of chloride. In summary, the plasma membrane fraction of the human kidney cortex and medulla contains a H+-ATPase, which is similar to the H+-ATPase described in other species, and we postulate that this H+-ATPase may be involved in urinary acidification.

Adenosine Triphosphate↗
PubMed2005

Lithium-induced NDI in rats is associated with loss of alpha-ENaC regulation by aldosterone in CCD.

Lithium-induced nephrogenic diabetes insipidus (Li-NDI) is associated with increased urinary sodium excretion and decreased responsiveness to aldosterone and vasopressin. Dysregulation of the epithelial sodium channel (ENaC) is thought to play an important role in renal sodium wasting. The effect of 7-day aldosterone and spironolactone treatment on regulation of ENaC in rat kidney cortex was investigated in rats with 3 wk of Li-NDI. Aldosterone treatment of rats with Li-NDI decreased fractional excretion of sodium (0.83 +/- 0.02), whereas spironolactone did not change fractional excretion of sodium (1.10 +/- 0.11) compared with rats treated with lithium alone (1.11 +/- 0.05). Plasma lithium concentration was decreased by aldosterone (0.31 +/- 0.03 mmol/l) but unchanged with spironolactone (0.84 +/- 0.18 mmol/l) compared with rats treated with lithium alone (0.54 +/- 0.04 mmol/l). Immunoblotting showed increased protein expression of alpha-ENaC, the 70-kDa form of gamma-ENaC, and the Na-Cl cotransporter (NCC) in kidney cortex in aldosterone-treated rats, whereas spironolactone decreased alpha-ENaC and NCC compared with control rats treated with lithium alone. Immunohistochemistry confirmed increased expression of alpha-ENaC in the late distal convoluted tubule and connecting tubule and also revealed increased apical targeting of all three ENaC subunits (alpha, beta, and gamma) in aldosterone-treated rats compared with rats treated with lithium alone. Aldosterone did not, however, affect alpha-ENaC expression in the cortical collecting duct (CCD), which showed weak and dispersed labeling similar to that in rats treated with lithium alone. Spironolactone did not affect ENaC targeting compared with rats treated with lithium alone. This study shows a segment specific lack of aldosterone-mediated alpha-ENaC regulation in the CCD affecting both alpha-ENaC protein expression and trafficking, which may explain the increased sodium wasting associated with chronic lithium treatment.

Aldosterone↗
PubMed1996

Mechanism of the thesaurismosis and altered lysosomal dynamics induced by poly-D-glutamic acid in kidney proximal tubular cells.

In the companion paper, we report that a single injection of poly-D-glutamic acid causes an acute lysosomal storage condition and apparently impairs the lysosomal fission dynamics. The present paper addresses the mechanisms of these two alterations using a combination of in vivo and in vitro biochemical approaches. After a single intravenous injection, 14C-poly-D-glutamic acid was rapidly cleared from the plasma and appeared in the urine. Yet, a small but sizable fraction of the injected polymer was taken up by the kidney cortex through a saturable process (Kuptake, 150 mg/kg body wt; uptakemax 96 micrograms/g cortex). Analytical subcellular fractionation of cortex homogenates demonstrated that at initial stages, the 14C label was predominantly associated with subcellular particles of intermediate size and low equilibrium density, and was therefore slowly transferred to larger particles equilibrating at high density, then codistributing with the lysosomal hydrolases. At a concentration of 10 mg/ml (equivalent to its estimated concentration in lysosomes), poly-D-glutamic acid formed micronic aggregates ( > or = 10 microns) when brought to solution at pH < or = 6 in relation to its decreased ionization (pKa of lateral chains approximately equal to 4.25). Finally, 1 day after the injection of poly-D-glutamic acid, the activities of several lysosomal enzymes (hexosaminidase, cathepsin B, acid sphingomyelinase, and sulfatase B), but not of all of them (eg, acid phosphatase), were increased in the kidney cortex. We propose that poly-D-glutamic acid reaches lysosomes by adsorptive endocytosis and becomes concentrated within these organelles because its withstands hydrolysis until it forms aggregates or precipitates, causing a decrease in the fluidity or the deformability ("gelling") of the lysosomal matrix. This should alter the dynamics of intercommunication of these organelles by impairing their fission without a proportionate effect on their fusion properties. In addition, the data suggest that the presence of poly-D-glutamic acid directly or indirectly slows down the degradation of several lysosomal enzymes.

Animals↗
PubMed1999

Stimulatory effect of regucalcin on proteolytic activity in rat renal cortex cytosol: involvement of thiol proteases.

The effect of regucalcin, a calcium-binding protein, on neutral proteolytic activity in the cytosol of rat kidney cortex was investigated. Proteolytic activity was significantly increased in the presence of regucalcin (0.01-0.25 microM) in the enzyme reaction mixture. This increase was not significantly altered by the addition of CaCl, (0.01 and 1.0 mM) or EGTA (1.0 mM), indicating that the effect of regucalcin was independent on Ca2+. The effect of regucalcin to increase proteolytic activity was completely prevented in the presence of N-ethylmaleimide (5 mM), a modifying reagent of thiol groups. Proteolytic activity was clearly elevated by dithiothreitol (5 mM). This elevation was further enhanced by regucalcin (0.1 microM). Meanwhile, the stimulatory effect of regucalcin on proteolytic activity was not significantly altered in the presence of diisopropylfluorophosphate (2.5 mM), an inhibitor of serine proteases. Also, the regucalcin effect was not appreciably changed by the addition of EDTA (2.5 mM), a chelator of metal ions, indicating that it is not involved in metal-related proteases. These results demonstrate that regucalcin can increase proteolytic activity in the cytosol of rat kidney cortex. Regucalcin may activate thiol proteases independent on Ca2+.

Animals↗
PubMed1978

A study of regulation of gluconeogenesis and the supply of cytosolic reducing equivalents for lactate formation in rat kidney-cortical-tubule fragments incubated with pyruvate.

1. Tubule fragments were isolated after treatment of rat kidney cortex with collagenase. The formation of glucose and lactate on incubation with 5mM-pyruvate was then measured under various conditions. 2. When tubule fragments were isolated from fed rats in the absence of Ca2+ and then incubated with various Ca2+ concentrations, an incubation period of 15--30 min was necessary to establish a metabolic steady state. Under these conditions glucose formation was increased by Ca2+, adrenaline or 3':5'-cyclic AMP to a greater extent than was lactate formation. Data show that appreciable lactate formation could not have resulted from glycolytic metabolism of glucose formed by gluconeogenesis during incubation. 3. When tubule fragments were isolated from fed rats in the presence of 1.27 mM-Ca2+ and adjustments made to the Ca2+ concentration at the commencement of incubation, metabolic steady state was rapidly established. Under these conditions lactate formation was almost insensitive to Ca2+ concentration (0.16--4.5 mM), whereas glucose formation varied with Ca2+ concentration in a sigmoidal manner. 3':5'-Cyclic AMP decreased this sigmoidicity. 4. Ca2+ depletion of the tissue before incubation appeared to change permanently the relationship between extracellular Ca2+ concentration and the measured rates of metabolic processes. 5. Under conditions of metabolic steady state, glucose formation by tubule fragments from fed rats was less sensitive than lactate formation to inhibition by 3-mercaptopicolinate or 2-n-butylmalonate. Lactate formation by tubule fragments prepared from 48 h-starved rats was more sensitive to these inhibitors. 6. Estimates were made of the rate of futile cycling of C3 species through pyruvate kinase. This was greater in the starved than in the fed state, was decreased by 3':5'-cyclic AMP in both the fed and the starved state, but was unaffected by Ca2+. 7. These results suggested that formation of lactate and glucose is less tightly linked in kidney cortex than in liver. A considerable amount of the supply of reducing equivalents for lactate formation did not appear to be associated with an energy-dependent translocation from mitochondria to cytosol involving a pyruvate leads to oxaloacetate leads to phosphoenolpyruvate leads to pyruvate cycle.

Aminooxyacetic Acid↗
PubMedDate not supplied

[Dynamics of the establishment of renal glomerular filtration in dogs during the early postnatal period].

By means of inulin clearance method, studies have been made on the glomerular filtration rate in 1-35-day puppies and adult dogs. The filtration rate was calculated per body weight, body surface, wet and dry weight of the kidney, wet and dry weight of the kidney cortex. It was found that dry weight of the kidney cortex is the best basis for comparison of the glomerular filtration in growing and adult organisms, as well as for the investigation of the development of this function.

Animals↗
PubMed1979

Metabolism of isolated kidney tubules. Interactions between lactate, glutamine and oleate metabolism.

Kidney-cortex tubule suspensions were prepared by collagenase treatment of kidney cortex from fed and starved rats. This preparation, consisting mainly of proximal convoluted tubules was incubated with three major renal substrates, L-lactate, glutamine and oleate to study the dose dependence of substrate uptake rates from medium substrate combinations. All three substances, when added at near physiological concentrations, modified the uptake rate and fate of the other substrates. In accordance with previous observations, oleate inhibited lactate uptake, and lactate decreased glutamine metabolism. Glutamine on the other hand led to a marked increase in lactate uptake. Both, glutamine and lactate increased oleate metabolism. Glucose was the main product of lactate and glutamine metabolism, lactate being preferentially taken up for this process. Oleate led to a net synthesis of triglycerides in the tubules, which was stimulated by the addition of lactate and glutamine. More than 75% of the oleate taken up was recovered as triglycerides. In the absence of fatty acids, triglyceride content of tubules decreased. The results indicate that oleate is taken up in preference to lactate and glutamine when all three substrates are offered to the tubule. Glucose and triglycerides are the main metabolic products of tubular substrate metabolism. Whereas glucose is released into the medium, triglycerides are stored in the tubule cell.

Animals↗
PubMed1967

Some properties of lactate dehydrogenase found in human urine.

1. Urinary lactate dehydrogenase was concentrated and subjected to starchblock electrophoresis. The isoenzyme pattern obtained was shown to be similar to that of the kidney cortex and medulla but different from that of the bladder and kidney pelvis. 2. The values for the relative activity and Michaelis constant of urinary lactate dehydrogenase were similar to those for kidney cortex and medulla but significantly different from those obtained for bladder and kidney pelvis. 3. The molecular weight of urinary lactate dehydrogenase was estimated by thin-layer chromatogtaphy on Sephadex G-200. The values obtained for several samples of urine ranged from 129 000 to 155 000 and were very close to that of the crystalline rabbit-muscle enzyme (140 000). 4. The question of the possible origin of urinary lactate dehydrogenase is discussed and the conclusion drawn that the kidney and not the plasma is the most likely source.

Chemical Phenomena↗
PubMed2001

Human kidney tubules detoxify chloroacetaldehyde, a presumed nephrotoxic metabolite of ifosfamide.

The nephrotoxic effects of the antineoplastic drug ifosfamide have been attributed to its hepatic metabolite chloroacetaldehyde. The effects of chloroacetaldehyde on isolated human kidney cortex tubules metabolizing lactate (a physiologic substrate in human kidneys) were investigated. At concentrations of > or =0.5 mM, chloroacetaldehyde was toxic to the human kidney tubules, as demonstrated by a dramatic decrease in cellular ATP levels and a large increase in lactate dehydrogenase release; chloroacetaldehyde also stimulated pyruvate accumulation and inhibited lactate removal and glucose synthesis. These effects, which were associated with incomplete disappearance of chloroacetaldehyde and extensive depletion of the cellular CoA, acetyl-CoA, and glutathione contents, were prevented by the addition of thiol-protecting drugs (mesna and amifostine). Human kidney tubules were demonstrated to metabolize chloroacetaldehyde at high rates, presumably via aldehyde dehydrogenase, which is very active in human kidneys. Carbon-13 nuclear magnetic resonance spectroscopy measurements indicated that human kidney tubules converted [2-(13)C]chloroacetaldehyde to [2-(13)C]chloroacetate, the further metabolism of which was very limited. At equimolar concentrations, chloroacetate was much less toxic than chloroacetaldehyde, indicating that chloroacetate synthesis from chloroacetaldehyde by human kidney tubules represents a detoxification mechanism that could play a role in vivo in preventing or limiting the nephrotoxic effects observed during ifosfamide therapy.

Acetaldehyde↗
PubMed1998

Inhibitory effect of calcium-binding protein regucalcin on protein kinase C activity in rat renal cortex cytosol.

The effect of regucalcin, a calcium-binding protein, on Ca2+-and phospholipid-dependent protein kinase (protein kinase C) activity in the cytosol of rat kidney cortex was investigated. With increasing concentrations of Ca2+, phosphatidylserine or dioctanoylglycerol in the reaction mixture, regucalcin (10[-8] M) caused a remarkable inhibition of protein kinase C activity. Regucalcin did not have a significant effect on protein kinase C activity in the presence of phosphatidylserine or dioctanoylglycerol without Ca2+ addition. Moreover, regucalcin significantly inhibited phorbol 12-myristate 13-acetate (PMA)-increased protein kinase C activity. Meanwhile, staurosporine (10[-9] M) caused a significant inhibition of protein kinase C activity. This inhibition was further enhanced by regucalcin addition. Regucalcin itself did not have protein kinase activity in either the presence or the absence of both Ca2+ and phospholipids. These results clearly indicate that regucalcin has an inhibitory effect on protein kinase C activity in the cytosol of rat kidney cortex. This inhibitory effect may be partly due to the regucalcin-induced Ca2+ binding.

Animals↗
PubMed1995

Identification of a novel ATP-dependent proteolytic activity in mitochondrial intermembrane space.

The formation of primary amines via proteolysis was monitored in isolated rat liver, kidney cortex and heart mitochondria in the presence and in the absence of ATP. The highest proteolytic activity was detected in kidney cortex mitochondria with about 120 nmoles primary amines/hour x mg protein. The formation rates of liver mitochondria amounted to about 100 nmoles primary amines/hour x mg protein and in heart mitochondria about 60 nmoles primary amines/hour x mg protein. In all mitochondria investigated an ATP-dependent proteolysis of 20-40 nmoles primary amines/hour x mg protein was detected. The effects of various protease inhibitors were tested in rat liver mitochondria and thiol-specific reagents showed a 35-70% inhibition. The ATP stimulable portion of proteolysis was blocked by hemin, a known inhibitor of ATP-dependent proteases. The localization of the proteolytic activity was tested by fractionation of the compartments of rat liver mitochondria using the flourogenic peptide suc-Leu-Leu-Val-Tyr-MCA as substrate. About 90% of the ATP-dependent peptide cleavage activity were found in the mitochondrial intermembrane space. The characteristics of the enzyme were compared to those of other known mitochondrial ATP-dependent proteases and it was concluded that it represents a novel proteolytic system of the intermembrane space.

ATP-Dependent Proteases↗
PubMed2004

MR imaging relaxation times of abdominal and pelvic tissues measured in vivo at 3.0 T: preliminary results.

PURPOSE: To measure T1 and T2 relaxation times of normal human abdominal and pelvic tissues and lumbar vertebral bone marrow at 3.0 T. MATERIALS AND METHODS: Relaxation time was measured in six healthy volunteers with an inversion-recovery method and different inversion times and a multiple spin-echo (SE) technique with different echo times to measure T1 and T2, respectively. Six images were acquired during one breath hold with a half-Fourier acquisition single-shot fast SE sequence. Signal intensities in regions of interest were fit to theoretical curves. Measurements were performed at 1.5 and 3.0 T. Relaxation times at 1.5 T were compared with those reported in the literature by using a one-sample t test. Differences in mean relaxation time between 1.5 and 3.0 T were analyzed with a two-sample paired t test. RESULTS: Relaxation times (mean +/- SD) at 3.0 T are reported for kidney cortex (T1, 1,142 msec +/- 154; T2, 76 msec +/- 7), kidney medulla (T1, 1,545 msec +/- 142; T2, 81 msec +/- 8), liver (T1, 809 msec +/- 71; T2, 34 msec +/- 4), spleen (T1, 1,328 msec +/- 31; T2, 61 msec +/- 9), pancreas (T1, 725 msec +/- 71; T2, 43 msec +/- 7), paravertebral muscle (T1, 898 msec +/- 33; T2, 29 msec +/- 4), bone marrow in L4 vertebra (T1, 586 msec +/- 73; T2, 49 msec +/- 4), subcutaneous fat (T1, 382 msec +/- 13; T2, 68 msec +/- 4), prostate (T1, 1,597 msec +/- 42; T2, 74 msec +/- 9), myometrium (T1, 1,514 msec +/- 156; T2, 79 msec +/- 10), endometrium (T1, 1,453 msec +/- 123; T2, 59 msec +/- 1), and cervix (T1, 1,616 msec +/- 61; T2, 83 msec +/- 7). On average, T1 relaxation times were 21% longer (P <.05) for kidney cortex, liver, and spleen and T2 relaxation times were 8% shorter (P <.05) for liver, spleen, and fat at 3.0 T; however, the fractional change in T1 and T2 relaxation times varied greatly with the organ. At 1.5 T, no significant differences (P >.05) in T1 relaxation time between the results of this study and the results of other studies for liver, kidney, spleen, and muscle tissue were found. CONCLUSION: T1 relaxation times are generally higher and T2 relaxation times are generally lower at 3.0 T than at 1.5 T, but the magnitude of change varies greatly in different tissues.

Abdomen↗
PubMedDate not supplied

Selenium in human tissues from New Zealand.

Selenium concentrations were measured in tissue samples obtained at autopsy from 45 New Zealand residents aged 4 months to 74 yr. Materials included liver, kidney cortex, skeletal muscle, heart, lung, and spleen. Samples of liver and brain were obtained from 16 fetuses (gestational ages, 27-42 wk). Except for kidney cortex, which contained high levels, concentrations of selenium were similar to those reported in other low-selenium areas, and lower than values obtained in selenium-adequate localities.

Adolescent↗
PubMed2003

Low endogenous glucocorticoid allows induction of kidney cortical cyclooxygenase-2 during postnatal rat development.

In postnatal weeks 2-4, cyclooxygenase-2 (COX-2) is induced in the rat kidney cortex where it is critically involved in final stages of kidney development. We examined whether changes in circulating gluco- or mineralocorticosteroids or in their renal receptors regulate postnatal COX-2 induction. Plasma corticosterone concentration peaked at birth, decreased to low levels at days 3-13, and increased to adult levels from day 22. Aldosterone peaked at birth and then stabilized at adult levels. Gluco- and mineralocorticoid receptor (GR and MR) mRNAs were expressed stably in kidney before, during, and after COX-2 induction. 11 beta-hydroxysteroid dehydrogenase 2 was induced shortly after birth and was widely distributed in the whole collecting duct system in the suckling period and then returned to an adult pattern. Supplementation with corticosterone (20 mg.kg-1.day-1) or GR-specific dexamethasone (1 mg.kg-1.day-1) during low endogenous corticosterone suppressed renal COX-2 mRNA and protein and led to a restricted distribution of COX-2 immunolabeling. The ability of glucocorticoids to affect COX-2 was reflected in colocalization of GR-alpha and COX-2 immunoreactivity and mRNAs in thick ascending limb of Henle's loop. The MR antagonist potassium canrenoate (20 mg.kg-1.day-1) enhanced COX-2 expression from days 5 to 10, but low MR-specific concentrations of DOCA (1 mg.kg-1.day-1) had no effect on COX-2. Renomedullary interstitial cells expressed GR-alpha and COX-2. Dexamethasone suppressed COX-2 in these cells. Thus low plasma concentrations of corticosterone allowed for cortical and medullary COX-2 induction during postnatal kidney development. Increased circulating glucocorticoid in the postnatal period may damage late renal development through inhibition of COX-2.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed1984

The influence of permanent adrenalin application on the triacylglycerol concentration and fatty acid synthesis in various tissues of the rat.

Adrenalin tablets (15 mg) or placebos were implanted into the neck of male Sprague-Dawley rats weighing between 150 to 250 g. 18 hours after implantation a significant lipolysis as well as enhanced concentrations of triacylglycerol in liver, kidney cortex and skeletal muscle can be observed in adrenalin treated rats. Measurements of fatty acid synthesis (3H method) in these tissues indicate that in kidney cortex and liver there is no contribution of local synthesis to elevated triacylglycerol content. In skeletal muscle local synthesis seems to be efficient to some degree. The main cause for lipid deposition in adrenalin supplied rats is, therefore, uptake of free fatty acids from the blood and following esterification with glycerol.

Animals↗
PubMed1983

Evidence for vitamin D dependent gamma-carboxylation in osteocalcin related proteins.

The content of gamma-carboxyglutamic acid (gla) was determined in rat femoral bone and kidney cortex in rachitic and vitamin D treated animals. It was demonstrated that the level of gla is decreased in vitamin D depleted animals both in kidney cortex and femoral bone. Supplementation of vitamin D deprived animals with this vitamin resulted in an increase in the gla concentration to almost normal levels. Also the incorporation of 14C NaHCO3 in renal cortex microsomes from rachitic animals was blocked. It is suggested that the absence of gla resulted from the direct action of vitamin D on mRNA for the Ca-binding protein.

1-Carboxyglutamic Acid↗