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 1,405 records · Page 78Linked to original sources
PubMed1977

Effect of oxygen and solute on PGE and PGF production by rat kidney slices.

Increasing oxygen from 5% to 95% resulted in an increases production of both PGE's and PGF's. The release of prostaglandins from slices of rat kidney cortex and outer and inner medulla was measured. Prostaglandin production was observed predominantly in the inner medulla, was close to the lower limit of detection in the outer medulla, and was undetectable in the cortex. Increasing oxygen concentration resulted in a threefold increase in inner medullary prostaglandin production. Synthesis at 95% O2 was less at 2100 mOsm than at 300 mOsm, while synthesis at 5% O2 was not affected by high solute concentration. The implications of these results with respect to kidney function are discussed.

Animals↗
PubMed1986

Metabolic and ultrastructural aspects of experimental diabetic glomerulopathy.

The effects of alloxan induced diabetes and insulin treatment on rat kidney glomerular ion transport and the oxidative phosphorylation were investigated in order to correlate metabolic and ultrastructural alterations. In alloxan diabetic rats an early decrease of Na+K+ ATPase activity in isolated glomeruli preparations and the subsequent uncoupling of oxidative phosphorylation were observed. These metabolic alterations are associated with structural changes such as the thickening of the basement membrane and the disorganization of both endothelial and mesangial cells. Insulin treatment induces a slow and only partial recovery of metabolic changes. Ultrastructural features of the kidney cortex were almost completely normalized after only two months of insulin treatment.

Animals↗
PubMed2006

Imaging endothelin ET(B) receptors using [18F]-BQ3020: in vitro characterization and positron emission tomography (microPET).

The endothelin (ET) receptor system has been shown to play a role in a number of vascular diseases. We have synthesized 18F-and 11C-labeled radioligands to enable in vivo imaging of the fundamental processes involved in ET receptor pharmacology in normal and diseased tissue using positron emission tomography (PET). One aim is to elucidate the proposed role of the ET(B) subtype as clearing receptor, removing ET-1 from the circulation, and whether this is an important mechanism to limit the detrimental effects caused by upregulated ET-1 in disease. To image ET(B) receptors we have labeled the selective agonist BQ3020 with 18F. In vitro characterization verified that [18F]-BQ3020 bound with a single subnanomolar affinity (K(D) = 0.34 +/- 0.10 nM, B(max) = 9.23 +/- 3.70 fmol/mg protein) to human left ventricle. Binding of [18F]-BQ3020 to human kidney was inhibited by ET-1 and unlabeled BQ3020 but not by the ET(A) selective antagonist FR139317, confirming that selectivity for the ET(B) receptor was retained. In vitro autoradiography revealed, as expected, high levels of ET(B) receptor densities in lung and kidney medulla, whereas kidney cortex and heart showed lower levels of ET(B) receptor densities. Furthermore, a high level of [18F]-BQ3020 binding was found to colocalize to macrophages in atherosclerotic coronary arteries. MicroPET studies demonstrated high uptake of [18F]-BQ3020 in ET(B) receptor-rich tissue, including lung, liver and kidney. The in vivo biodistribution of [18F]-BQ3020 was comparable to that previously obtained for [18F]-ET-1, supporting our hypothesis that the ET(B) receptor plays a significant role in the uptake of ET-1. In conclusion, [18F]-BQ3020 has retained high affinity and selectivity, allowing imaging of ET(B) receptor distributions in vitro and in vivo in human and animal tissue. Furthermore, in vitro data suggest that [18F]-BQ3020 potentially can be used to image atherosclerotic lesions in vivo using PET.

Animals↗
PubMed2005

Arterial spin labeling blood flow magnetic resonance imaging for the characterization of metastatic renal cell carcinoma(1).

RATIONALE AND OBJECTIVE: This study sought to assess the feasibility of arterial spin labeling (ASL) blood flow (BF) magnetic resonance imaging (MRI) for the study of metastatic renal cell carcinoma (RCC) in the body, where the respiratory, cardiac, and peristaltic motions present challenges when applying ASL. MATERIALS AND METHODS: ASL was performed using a background-suppressed single-section flow-alternating inversion recovery (FAIR) preparation and a single-shot fast spin-echo imaging sequence on a 3.0-T whole body imager. Tumor BF was evaluated for 26 patients with RCC metastatic to the liver, bone, lung, or lymph nodes before VEGF receptor inhibitor therapy. Two cases with tumor size change after treatment were also scanned 1 month after therapy. For validation, kidney cortex BF in five normal volunteers was measured with the same technique and compared with literature values. RESULTS: ASL was successfully performed in all normal volunteers and in 20 of 26 patients. The six failures resulted from a systematic error, which can be avoided in future studies. For normal volunteers, measured kidney cortex BF was 275 +/- 14 mL/min/100 g, a value consistent with the literature. ASL determined tumor BF averaged across tumor volume and subjects was 194 mL/min/100 g (intersubject SD = 100), resulting in high perfusion signal and conspicuity of lesions. Bright signal was also seen in large vessels and occasionally in bowel. In the two cases studied 1 month after therapy, ASL perfusion changes were consistent with tumor size changes. CONCLUSION: With background suppression, ASL MRI is a feasible method for quantifying BF in patients with renal cell carcinoma. This technique may be useful for evaluating tumor response to antiangiogenic agents.

Antineoplastic Agents↗
PubMedDate not supplied

Polyamines regulate calcium fluxes in a rapid plasma membrane response.

Activation of cell-surface receptors often evokes changes in Ca2+ fluxes leading to an increase in cytosolic Ca2+, a generally accepted mediator of many cell responses. The molecular mechanisms by which surface agonists elicit these changes in Ca2+ flux have remained elusive. An increase in the polyamines putrescine, spermidine and spermine, and their rate-regulating, synthetic enzyme ornithine decarboxylase (ODC), is one of the earliest events that occur during cell growth, replication and differentiation. However, the precise physiological roles of the polyamines remain enigmatic. Recently, we found that testosterone induces an early (less than 60s), Ca2+- and receptor-dependent stimulation of endocytosis, hexose transport and amino acid transport in mouse kidney cortex involving the proximal tubules. This response is associated with increased Ca2+ fluxes and a mobilization of intracellular calcium, and is thought to represent a direct, receptor-mediated action of testosterone on the surface membrane. Polyamine synthesis was previously found to be essential for the long-term effects of testosterone on mouse kidney. We now report that testosterone evokes a rapid (less than 30 s), transient increase in ODC activity and a sustained increase in polyamines in kidney cortex. This polyamine synthesis is obligatory for stimulation of membrane transport functions and Ca2+ fluxes. These findings form the basis for a new theory of information flow in stimulus-response coupling in which the polyamines serve as messengers to generate a Ca2+ signal by increasing Ca2+ influx and mobilizing intracellular calcium via a cation-exchange reaction.

Animals↗
PubMed2003

PDZK1: II. an anchoring site for the PKA-binding protein D-AKAP2 in renal proximal tubular cells.

BACKGROUND: PDZK1, a multiple PDZ protein, was recently found to interact with the type IIa Na/Pi cotransporter (NaPi-IIa) in renal proximal tubular cells. In a preceding study, yeast two-hybrid screens using single PDZ domains of PDZK1 as baits were performed. Among the identified proteins, a C-terminal fragment of the dual-specific A-kinase anchoring protein 2 (D-AKAP2) was obtained by screening PDZ domain 4. METHODS: After its molecular cloning by means of RACE, the renal expression of D-AKAP2 was analyzed by real-time polymerase chain reaction (PCR) and immunohistochemistry. Protein interactions were characterized by overlays, pull-downs, and immunoprecipitations from transfected opossum kidney (OK) cells. RESULTS: Based on 5'-RACE and PDZK1 overlays of mouse kidney cortex separated by two-dimensional electrophoresis, it was suggested that the renal isoform of D-AKAP2 in mouse comprises 372 amino acids and exists as a protein of >40 kD. Immunohistochemistry and real-time PCR localized D-AKAP2 only to the subapical pole of proximal tubular cells in mouse kidney. In pull-down experiments, D-AKAP2 tightly bound PDZK1 as well as N+/H+ exchanger regulator factor (NHERF-1), but the latter with an apparent fourfold lower affinity. Similarly, His-tagged D-AKAP2 specifically retained PDZK1 from mouse kidney cortex homogenate. In addition, myc-tagged D-AKAP2 and HA-tagged PDZK1 co-immunoprecipitated from transfected OK cells. CONCLUSION: We conclude that D-AKAP2 anchors protein kinase A (PKA) to PDZK1 and to a lesser extent to NHERF-1. Since PDZK1 and NHERF-1 both sequester NaPi-IIa to the apical membrane, D-AKAP2 may play an important role in the parathyroid hormone (PTH)-mediated regulation of NaPi-IIa by compartmentalization of PKA.

A Kinase Anchor Proteins↗
PubMed1978

Studies on the orientation of brush-border membrane vesicles.

Orientation of rat renal and intestinal brush-border membrane vesicles was studied with two independent methods: electron-microscopic freeze-fracture technique and immunological methods. With the freeze-fracture technique a distinct asymmetric distribution of particles on the two membrane fracture faces was demonstrated; this was used as a criterion for orientation of the isolated membrane vesicles. For the immunological approach the accessibility or inaccessibility of aminopeptidase M localized on the outer surface of the cell membrane to antibodies was used. With both methods we showed that the brush-border membrane vesicles isolated from rat kidney cortex and from rat small intestine for transport studies are predominantly orientated right-side out.

Alanine↗
PubMed1976

[Effect of retabolil on renal tubular secretion].

Chronic experiments on dogs and rats showed retabolil, an anabolic steroid (given in a dose of 2-5 mg/kg for 7 days) to produce an increase in renal tubular secretion of cardiotrast. Rats displayed a simultaneous elevation in the content of protein and RNA in the kidney cortex. The data obtained were interpreted from the aspect of protein nature of carriers taking part in the renal secretory transport.

Anabolic Agents↗
PubMed1999

Effect of experimentally induced hypothyroidism on sulfate renal transport in rats.

Decreased serum sulfate concentrations are observed in hypothyroid patients. However, the mechanism involved in thyroid hormone-induced alterations of renal sulfate homeostasis is unknown. The objectives of this investigation were to determine the effect of 6-propyl-2-thiouracil (PTU)-induced hypothyroidism in rats on 1) the in vivo serum concentrations, renal clearance, and renal reabsorption of sulfate, 2) the in vitro renal transport in brush-border membrane (BBM) and basolateral membrane (BLM) vesicles, and 3) the cellular mechanism of the hypothyroid-induced alteration in sulfate renal transport. Serum sulfate concentrations, renal fractional reabsorption of sulfate, and creatinine clearance were decreased significantly in the hypothyroid group. The Vmax values for sodium-sulfate cotransport in BBM were significantly decreased in the kidney cortex from the hypothyroid animals (0.90 +/- 0.31 vs. 0.49 +/- 0.08 nmol. mg-1. 10 s-1, n = 5-6, P < 0.05) without changes in Km. There were no significant differences in Vmax and Km for sulfate/anion exchange transport in BLM. Sodium-dependent sulfate transporter (NaSi-1) mRNA and protein levels were significantly lower in the kidney cortex from hypothyroid rats. Hypothyroidism did not alter the membrane motional order (fluidity) in BBM and BLM, which indicates that the changes in the membrane fluidity do not represent the mechanism for the altered renal transport. These results demonstrate that PTU-induced hypothyroidism decreases sodium-sulfate cotransport by downregulation of the NaSi-1 gene.

Animals↗
PubMed2006

Calpain activation and secretion promote glomerular injury in experimental glomerulonephritis: evidence from calpastatin-transgenic mice.

Glomerular injury and albuminuria in acute glomerulonephritis are related to the severity of inflammatory process. Calpain, a calcium-activated cysteine protease, has been shown to participate in the development of the inflammatory process. Therefore, for determination of the role of calpain in the pathophysiology of acute glomerulonephritis, transgenic mice that constitutively express high levels of calpastatin, a calpain-specific inhibitor protein, were generated. Wild-type mice that were subjected to anti-glomerular basement membrane nephritis exhibited elevated levels of calpain activity in kidney cortex at the heterologous phase of the disease. This was associated with the appearance in urine of calpain activity, which originated potentially from inflammatory cells, abnormal transglomerular passage of plasma proteins, and tubular secretion. In comparison with nephritic wild-type mice, nephritic calpastatin-transgenic mice exhibited limited activation of calpain in kidney cortex and limited secretion of calpain activity in urine. This was associated with less severe glomerular injury (including capillary thrombi and neutrophil activity) and proteinuria. There was a reduction in NF-kappaB activation, suggesting that calpain may participate in inflammatory lesions through NF-kappaB activation. There also was a reduction in nephrin disappearance from the surface of podocytes, indicating that calpain activity would enhance proteinuria by affecting nephrin expression. Exposure of cultured podocytes to calpain decreased nephrin expression, and, conversely, exposure of these cells to calpastatin prevented TNF-alpha from decreasing nephrin expression, demonstrating a role for the secreted form of calpain. Thus, both activation and secretion of calpains participate in the development of immune glomerular injury.

Albuminuria↗
PubMedDate not supplied

[Activity of glutamine deaminating enzymes in the kidneys, liver and serum of dogs with renal failure and under normal conditions].

Among all the glutamine deaminating enzymes the highest activity was exhibited by phosphate-dependent glutaminase (72% of the total activity) in kidney cortex and blood serum of healthy dogs and by phosphate-independent glutaminase (47% of the total activity)--in liver tissue. A distinct decrease in the activity of both isoforms of glutaminase I (phosphate-dependent and phosphate-independent enzymes) and of glutaminase II (pyruvate-dependent enzyme) occurred in kidney under conditions of acute and chronic kidney insufficiency. The phosphate-independent glutaminase activity was decreased and, by contrast, activities of phosphate- and pyruvate-dependent glutaminases were increased in liver tissue under the conditions of acute kidney insufficiency. In blood serum under conditions of acute and chronic insufficiency the glutaminase I (both forms) activity was distinctly dcreased, but the glutaminase II activity had a marked trend to elevation. Possible mechanisms responsible for an alteration of glutamine deaminating enzymes in kidney, liver tissue and blood serum of dogs under acute and chronic kidney insufficiency are discussed.

Animals↗
PubMed1989

Trace elements intake in the Faroe Islands. III. Element concentrations in human organs in populations from Bergen (Norway) and the Faroe Islands.

Flameless as well as flame atomic absorption spectrophotometry were used for the analysis of six elements (calcium, iron, zinc, selenium, cadmium and mercury) in human organs (liver, kidney cortex and medulla, heart, pancreas and spleen) from 13 bodies from Bergen and 10 from the Faroe Islands. Samples were taken at autopsy and the organs selected were without pathological signs. All patients were born between 1899 and 1923. Element concentrations in the organs studied were comparable to previous studies, except for high mercury and selenium values in the liver, the kidney cortex and medulla of subjects from the Faroe Islands. The high mercury and selenium values may be explained by the high consumption of pilot whales by the Faroe Islands population.

Aged↗
PubMed2003

Proximal convoluted tubules of the rats kidney--a stereological analysis.

BACKGROUND AND PURPOSE: The aim of this work was to order quantitative parameters of the proximal convoluted tubules (PCT) in the normal rat kidney cortex. Volume density (VV), both surface and specific surface density toward interstitium (SVi and SVi/VV) and toward lumen (SVl and SVl/VV) and thickness (T) of tubules epithelium have been stereologically ordered. MATERIAL AND METHODS: Stereologically were analysed 170 test fields by lattice L36 on the paraffin sections of the three adult male Wistar rats kidney dyeing by PAS-method. RESULTS: The mean values of the variables analysed were: VV=76.4 % +/-0.012; SVi=0.056 microm-1 +/-0.004; SVl=0.028 microm-1 +/-0.003; SVi/VV=0.073 microm-1 +/-0.003; SVl/VV=0.037 microm-1 +/-0.005; T=18,26 microm +/-0.897. CONCLUSIONS: Stereological methods are making a very valuable contribution to science over recent years. We have used unbiased stereological counting methods to obtain objective quantitative parameters of the PCT epithelium in the normal rats' kidney cortex.

Journal Article↗
PubMed1979

[On the localization of sorbitol dehydrogenase in the rat kidney (author's transl)].

We have investigated the localization and demonstration of sorbitol dehydrogenase activity in the rat kidney by comparative histochemical-electrophoretical technique. Under histochemical conditions an adequate demonstration of the activity of the sorbitol dehydrogenase in native sections is possible by membrane incubating technique in presence of PMS and KCN. In the glomerulum the strong and uniform reaction with regard to the specifity is not clear. In the glomerula of semithin sections from glutaraldehyde fixed, incubated and Epon-embedded cryostate sections the reaction product is localized predominantly in the maesangium cells. By micropolyacrylamidgel gradient electrophoresis of the supernatant from the kidney cortex and of isolated glomerula 2 sorbitol dehydrogenase fractions were found. The results are discussed in connection with the specifity of the reaction.

Animals↗
PubMed1967

Nutrition and lysosomal activity. The influence of vitamin E deficiency and its duration on the stability of lysosomes in the kidneys of rats.

1. Experiments on rats were made to find whether the increased liability of the kidney-cortex tubules to autolysis post mortem, which is a well-established abnormality in vitamin E deficiency, can be correlated with changes in lysosomal activity. Parallel observations were made on the development of certain other abnormalities characteristic of avitaminosis E. 2. In rats killed after long periods (8-10 months) of subsistence on a standard vitamin E-deficient diet, containing lard, both the rate of kidney autolysis post mortem and the enzyme activity of lysosome preparations from the fresh tissues were much greater than in controls. A greater percentage difference was usually found in the ;free' enzyme fraction than in ;bound' or ;total' activity. 3. In rats killed after graded periods (3-8 months) of deficiency, two abnormalities (decreased resistance of the erythrocytes to haemolysis, and brown discoloration of the uterus) were already evident at a stage (3-4 months) when the liability to rapid kidney autolysis had not begun. At this point the enzymic activity of kidney extracts differed little between deficient animals and controls given alpha-tocopherol. As the duration of deficiency advanced, parallel increases occurred in the rate of kidney autolysis and in lysosomal instability. 4. When cod-liver oil, rich in polyunsaturated fatty acids but freed from vitamin A, was substituted for lard in the diet, the time (1(1/2) months) required for the inducement of both rapid kidney autolysis and decreased lysosomal stability was greatly shortened. The time for the inducement of brown discoloration of the uterus was not shortened and the kidney abnormalities appeared while the uterus was still normal. 5. Confirmation was thus obtained for the view that the various tissues of the rat respond differently to the relationship between the adequacy of the vitamin E status and the intake of polyunsaturated fatty acids. The kidney-cortex tubules, as evidenced by autolysis post mortem and the corresponding decrease in lysosomal stability, may be classed among those tissues that are most sensitive to the effect of high intakes of polyunsaturated acids.

Animals↗
PubMed2005

Role of renal nitric oxide synthase in diabetic kidney disease during the chronic phase of diabetes.

BACKGROUND: Several studies have suggested that an early increase in renal nitric oxide (NO) production or activity mediates pathophysiologic and morphologic changes in diabetic nephropathy. To evaluate the role of NO in developing diabetic kidney disease, we studied the NO system in streptozotocin (STZ)-induced diabetic rats for a period of 8 weeks. METHODS: Control rats, STZ-induced diabetic rats, and STZ-induced diabetic rats treated with insulin were monitored and sacrificed at 1, 2, and 8 weeks. Urinary cGMP was measured, and the levels and activity of NO synthase (NOS) isoforms in the kidney cortex were determined at specific times by immunoblotting and diaphorase staining. RESULTS: Diabetic rats had increased kidney weight, urinary volume, glucose, sodium and potassium excretion, which was precluded by insulin treatment. Creatinine clearance was increased in the diabetic group and reversed by insulin treatment. Urinary cGMP decreased by 71, 93, and 92% at 1, 2, and 8 weeks of diabetes, respectively, compared with the control animals. Insulin treatment curtailed the urinary cGMP reduction in diabetic animals. Total NOS activity in the renal cortex was reduced by 65, 52, and 44% after 1, 2, and 8 weeks of diabetes, respectively, and returned to normal levels upon insulin treatment. NADPH diaphorase staining of renal cortical slices showed a 77, 63, and 70% decrease in neuronal NOS isoform activity in the macula densa after 1, 2, and 8 weeks of diabetes, respectively, compared with control non-diabetic animals. This reduction was normalized by insulin treatment. Endothelial NOS protein expression in the kidney cortex tended to increase after 1 week of diabetes and its level was elevated significantly after 2 and 8 weeks of diabetes. However, neuronal NOS protein expression in the kidney cortex was reduced by 52% in 2-week diabetic animals, but this reduction was normalized by insulin treatment. CONCLUSIONS: The decreased renal NOS activity during the late phase of diabetes is partially associated with a decrease in neuronal NOS activity and protein expression in kidney macula densa.

Animals↗
PubMed1987

Resistance to acute nephrotoxicity induced by cadmium-metallothionein dependence on pretreatment with cadmium chloride.

Three groups of rats (B-D) were given various daily doses of CdCl2 (0.5-2 mg Cd/kg) continuously or in intervals during time periods of 1-8 weeks. Another group of animals (A) were kept untreated. At the end of the period, selected subgroups of groups A-D were given a single subcutaneous injection of 109Cd-metallothionein (109CdMT) 0.05 or 0.4 mg Cd/kg ("challenge dose"). Subsequently, urinary creatinine, protein, Cd, 109Cd and MT and kidney cortex Cd, 109Cd and MT were determined. In group A (no long term pretreatment), an increased proteinuria was observed after the rats had received the lower of the challenge doses of 109CdMT, and an even greater increase after the higher challenge dose of 109CdMT. No such increase appeared in group B, C and D (repeatedly pretreated with CdCl2) at either of the challenge doses. Higher metallothionein concentrations in kidney cortex observed in the pretreated groups constitute a plausible explanation of the protective effects of pretreatment against the development of increased proteinuria after challenge dosing. It is likely that increasing Cd concentrations, gradually accumulating in the renal cortex (22-226 micrograms/g wet wt.) as a result of the pretreatment, served to induce the synthesis of metallothionein in the renal cortical cells, thus making them resistant to the challenge from 109CdMT.

Acute Disease↗