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At least 19 recordsLinked to original sources
PubMed1979

Nephrotoxicity of aminophenols: effects of 4-dimethylaminophenol on isolated rat kidney tubules.

In isolated rat kidney tubules DMAP was found to inhibit the gluconeogenesis from lactate, pyruvate, or dihydroxyacetone. The ratio DMAP/protein rather than the calculated concentration of DMAP determined the strength of the effect, 20--25 nmoles DMAP/mg protein inhibiting the rate of gluconeogenesis by about 50%. The inhibition was not reversible. Phenacetin, 4-aminophenol and 4-acetamidophenol were much less effective than DMAP in inhibiting gluconeogenesis in isolated rat kidney tubules. DMAP 14C-labeled in the ring was quickly bound to proteins in kidney tubules. A portion of DMAP which did not exceed about 4 nmoles/mg protein, was bound in compounds soluble in perchloric acid. From this portion tris-GS-DMAP was isolated. DMAP diminished the glutathione content of isolated rat kidney tubules. Reduced glutathione added before DMAP prevented the inhibition of gluconeogenesis and diminished the binding of DMAP to proteins. The binding of DMAP required oxygen and was inhibited by carbon monoxide or cyanide. Several enzymes from isolated kidney tubules were found to be inhibited by DMAP doses which inhibited gluconeogenesis. Large DMAP doses also diminished the sums of ATP + ADP + AMP as well as NAD + NADH and NADP + NADPH. This effect corresponded to an increase in nucleotide degradation products and to increased activity of extracellular LDH. The results indicate that the inhibition of gluconeogenesis by DMAP is not due to a specific effect on one enzyme or on membranes but to unspecific reactions with many substances.

Aminophenols↗
PubMed1977

Contribution of pH-sensitive metabolic processes to pH homeostasis in isolated rat kidney tubules.

The metabolism of isolated rat kidney tubules suspended in calcium-free physiological saline buffered with phosphate was found to be sensitive to changes in the pH of the suspending medium. Lowering the pH from 7.8 to 6.4 brought about increases in the rates of oxidation of added succinate, glutamate or glutamine as well as in the production of glucose from lactate, glutamine, succinate and fructose. The cellular ATP level was also higher in tubules incubated at pH 6.4 In contrast, the utilization of added glucose was greater at pH 7.8 than at pH 6.4, a substantial amount of lactate being produced at the higher pH. When glucose and either lactate or glutamine were provided as co-substrates glucose was the preferred fuel at pH 7.8 but the alternative substrate was the more readily utilized at pH 6.4. As a consequence of the metabolic activities of the tubules the pH of the suspending medium changed, utilization of lactate, glutamate or glutamine causing a rise in pH while conversion of glucose to lactate caused a fall in pH. In cases where two substrates were metabolized concurrently over a period of 3 h the extracellular pH tended towards a plateau level of approximately pH 7.4. It is proposed that pH-sensitive metabolism in isolated kidney tubules contributes to pH homeostasis in the cellular environment.

Adenosine Triphosphate↗
PubMed1978

Inhibition of gluconeogenesis in isolated rat kidney tubules by branched chain alpha-ketoacids.

Isolated rat kidney tubules served as a model to investigate the direct effects of branched chain aminoacids, their alpha-ketoderivatives, and of the homolog straight chain aliphatic alpha-ketoacids on renal gluconeogenesis. It is demonstrated that the alpha-ketoderivatives, rather than the branched chain aminoacids themselves, are potent inhibitors of renal gluconeogenesis from precursors, entering the glucogenic pathway on all levels below and above triose phosphate. This inhibitory action is not specific for the branched chain alpha-ketoacids, since it is also observed in the presence of the homolog straight chain aliphatic alpha-ketoacids. The suppression of renal gluconeogenesis by alpha-ketoacids can not be explained by a direct inhibition of gluconeogenic reactions, by inhibition of cellular respiration, or by interference with the stimulatory action of Ca++, cAMP, and L-lysine on renal gluconeogenesis. Although the point of inhibitory attack of alpha-ketoacids in renal gluconeogenesis could not be localized, an impairment of the kidney to respond to metabolic acidosis with an increase of gluconeogenesis was observed, since the pH optimum of renal gluconeogenesis was shifted from pH 6.8 to pH 7.7 in the presence of alpha-ketoisovaleric acid.

Amino Acids, Branched-Chain↗
PubMed1979

A phenomenologic evaluation of CO2-diffusion restriction in kidney tubules studied in an artificial membrane system.

The chemical course in a multi-membrane system with interacting H+ and HCO3 ions has been described phenomenologically as an analogy of the neutralisation reaction between secreted H+ and filtered HCO-3 ions in the proximal tubules of the kidney. It was shown that the produced CO2 gave the highest PCO2 in the asymmetrically placed reaction centre, which favours a build-up of a high intratubular PCO2. The CO2 transport was dependent on the rate-limiting permeation of the reacting ions, and the permeation could be increased by the influence of solutions of macromolecules such as carbonic anhydrase, albumin and dextran.

Bicarbonates↗
PubMed1979

[Regeneration of the proximal kidney tubules after sublimate-induced necrosis in the rate. Scanning electron microscopic studies].

Necrosis of the proximal tubules of the kidney in white rats has been produced by a relative small doses (1,5 mg/kg) of sublimate. Necrosis of the epithelial cells and their regeneration was studied during 10 days by scanning electron microscopy. Parallelism of the various regressive and regenerative processes was noted, attention was paid to the correlation existing between them. Periodicity of normal and necrotic segments was also observed. As a sequal of the necrosis the basement membranes became denuded, later in the first period of the regeneration flattened epithelial cells--having no microvilluses--covered them. On the surface of the latter, in a very short period (several hours) gradually microvilluses, regular brush-border and interdigitation of the cells were formed. In 10-17 days the regenerated epithelium could hardly be distinguished by scanning electron microscopy from the normal one.

Acute Kidney Injury↗
PubMed1976

Isolation of the basal and lateral plasma membranes of rat kidney tubule cells.

A method was developed to isolate renal basolateral membranes from cortical kidney tubule cells of single rats. The isolated membrane fraction was characterized by the measurement of marker enzyme activities and by electron microscopy. 1. After centrifugation of crude plasma membranes on a discontinuous sucrose density gradient the basolateral membranes accumulated at a sucrose density of p= 1.14-1.15 g/ml. The yield was 147 mug membrane protein/g kidney wet weight. Protein recovery was 0.1%. 2. (Na+ + K+)-ATPase was enriched 22-fold from the homogenate. The recovery was 2.6%. The (Na+ + K+)/Mg2+-ATPase ratio was 4.1. 3. The contamination by brush borders was small. Alkaline phosphatase was 1.6-fold enriched and 0.2% was recovered. Aminopeptidase was 1-fold enriched with a recovery of 0.1%. The contamination by mitochondria, lysosomes and endoplasmic reticulum was negligible. 4. In electron micrographs the basolateral membranes showed a typical triple layered profile and were characterized by the presence of junctional complexes, gap junctions or tight junctions.

Adenosine Triphosphatases↗
PubMedDate not supplied

The role of oxidation in the renal metabolism of glutamine by rat kidney tubules in vitro.

The metabolism of cold and 14C-[U]-glutamine in isolated kidney tubules of normal rats was studied in vitro to establish the relative importance of glucose synthesis and complete oxidation to CO2 for the metabolism of this amino acid in vitro. These metabolic fates were estimated by drawing a complete balance of the nitrogens and of the carbon chains of the extracted glutamine and studying the formation of 14CO2 from 14C-glutamine. It was found that glucose production constitutes the major fate for glutamine metabolism with 1 mM glutamine and that glutamine oxidation constitutes less than 20% of the metabolic fate of the carbon skeleton of this amino acid. With 5 or 10 mM glutamine however, the maximal oxidation to CO2 becomes more important (25%).

Animals↗
PubMed1979

Characteristics of glutamine metabolism by rat kidney tubules: a carbon and nitrogen balance.

The metabolism of glutamine by a suspension of rat kidney tubules was studied in vitro. The influence of duration of incubation, glutamine concentration, and metabolic state of the donor animals was investigated. The relative importance of glucose synthesis, amino acid production, and oxidation to CO2 was estimated by drawing a complete balance of the nitrogens and the carbon chains of the extracted glutamine. It was found that the initial (first 15 min) rate of glutamine utilization was significantly greater than the subsequent rate due to an initial, but transient, extracellular accumulation of glutamate. This phenomenon was suppressed when a small amount of glutamate was added to the incubation medium. Glucose production constitutes the major fate for glutamine metabolism. No net oxidation of glutamine could be detected with 1 mM glutamine during the first 30 min. However, glutamine oxidation becomes significant after prolonged incubation (16% at 120 min). The metabolic fate of glutamine differs when 5 or 10 mM are presented to the tubules, glutamate production and oxidation to CO2 becoming more important. Metabolic acidosis or a 48-h fast increases glutamine extraction and enhances its utilization glucose synthesis while they depress glutamate accumulation and oxidation to CO2. Metabolic alkalosis has the opposite effect. It is concluded that the metabolism of glutamine in vitro is dependent on the conditions of the study. Furthermore, total oxidation to CO2 is not a major fate for glutamine metabolism at physiological concentration and is not enhanced by acidosis in the rat kidney in vitro.

Amino Acids↗
PubMed1977

[Kidney tubule changes in the terminal stage of chronic glomerulonephritis].

The autopsy material was used for histological and histochemical study of lesions in tubules of the kidneys in chronic glomerulonephritis in comparison with those in acute renal insuffuciency (ARI) of various etiologies. In addition to the phenomena of intracellular regeneration in tubules of the functioning nephrons with formations of nephromas and tubule atrophy in the zone of glomerular sclerosis, some observations showed signs of insufficiency of cortical circulation. They were manifested in dystrophy of the proximal segment epithelium. Dystrophic changes are followed by regeneration which occurs at different times and runs an irregular course. Changes in the tubules are similar to those observed in the oligo-anuria stage of ARI. When cortical circulation is not compensated, paresis and collateral insufficiency develop. Small cortical necroses may be formed. All these changes, when they occur in extracapillary proliferation, may be manifested by the clinical symptocomplex of acute renal insufficiency.

Atrophy↗
PubMed1979

Effects of kidney tubule obstruction on glomerular function in rats.

The effects of chronic blockade of single kidney tubules on glomerular capillary pressure (GCP) and blood flow were examined in anesthetized rats. Tubule blockade with castor oil for 24 h decreased GCP from 48.0 +/- 3.8 to 39.5 +/- 4.7 mmHg (P less than 0.001). The full decrease in GCP observed at 24 h was apparent by about 12 h. Bilateral ureteral obstruction for 24 h prevented a decrease in GCP. Nonradioactive microspheres (8.4 +/- 0.84 micron diam) were used to assess relative blood flow to blocked and normal nephrons. These microspheres were completely extracted by rat kidneys and had no effect on total renal blood flow. The ratio of microsphere counts in glomeruli of blocked versus normal nephrons averaged 0.61 +/- 0.21, indicating a significantly (P less than 0.001) decreased glomerular blood flow in nephrons obstructed for 24 h. Since both GCP and blood flow were reduced after tubule obstruction, afferent arteriolar constriction is involved. The data suggest a local mechanism activated by prolonged tubule blockade which shifts filtrate formation and blood flow away from blocked nephrons.

Animals↗
PubMedDate not supplied

Effect of different preservation solutions and substrates on metabolic viability of kidney tubules.

Glucose production, pyruvate uptake and lactate production were taken as metabolic viability tests for isolated rat kidney tubules preserved in hypothermia. The results depend on the type of preservation solution used. Species specific serum is the only solution sustaining cellular metabolism at a normal level. Using Collins solution all viability parameters showed the lowest results. Addition of certain substrates to the Krebs-Henseledt solution improves metabolic viability.

Animals↗
PubMed1976

A kallikrein-specific inhibitor in rat kidney tubules.

A kallikrein inhibitor was found in tubules of the rat kidney and purified by chromatography on Sephadex G-100. The molecular weight of the inhibitor, estimated by gel filtration and dodecylsulfate electrophoresis, is about 4700. It inhibits the following kallikreins: porcine submanidbular and pancreatic kallikrein, rat kidney and urine kallikrein, and human urine and plasma kallikrein. An inhibition of bovine trypsin was not observed.

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↗
PubMed1978

Ultrastructure and segmentation of microdissected kidney tubules in the marine flounder, Pleuronectes platessa.

A new method combining electron microscopy with microdissection was used to study the segmental variation along the tubule of a marine flounder. Two different nephron types were present. One type had long tubules with the glomeruli located close to the kidney surface. The other type had shorter and more coiled tubules with the glomeruli located close to the terminal end of the same nephron. Five different segments were present: (1) neck segment, (2) first proximal segment, (3) second proximal segment, (4) third proximal segment, and (5) collecting tubule. The third proximal segment was not present in all tubules. An extensive system of infoldings from the plasma membrane was present in all segments, except the neck segment and the collecting tubule. Tight junctions impermeable to lanthanum were present in all segments. The collecting duct cells also had extensive infoldings from the plasma membrane and tight junctions impermeable to lanthanum were also present here.

Animals↗
PubMed1978

Regulation of pyruvate dehydrogenase by Ca2+, 3'5' cyclic AMP and adrenalin in isolated rat kidney tubules.

Renal pyruvate dehydrogenasea activity was measured in suspensions of kidney cortex tubules from fed rats after incubation with various concentrations of Ca2+, 3'5' cyclic AMP or adrenalin. At certain concentrations these agents all decreased pyruvate dehydrogenasea activity and increased glucose formation from pyruvate. There appeared to be some interdependence between the effects of Ca2+ and 3,5, cyclic AMP on pyruvate dehydrogenasea activity. Effects of adrenalin on pyruvate dehydrogenasea activity were no longer observed when palmitate was included in incubations. The possibility that regulation of pyruvate dehydrogenasea may indirectly contribute to the control of gluconeogenesis by influencing pyruvate metabolism is briefly discussed.

Animals↗
PubMedDate not supplied

[Succinate dehydrogenase and Na+-K+-ATPase activities in cells of rat kidney tubules during increased excretion of sodium, caused by furosemide].

In the cells of nephron tubules an effect of furosemide on kidney function and on succinate dehydrogenase and Na+-K+-ATPase activities was studied cytochemically. Administration of furosemide (1 mg per 100 g of body weight) increased excretion of sodium and potassium. If the rate of filtration through Malpighian tufts was constant, the increase in Na and K excretion demonstrated the tubular effect of the diuretics. Both administration of furosemide and preincubation of the drug with kidney slices in vitro caused a decrease in succinate dehydrogenase activity in the cells of all the nephron sections. These data suggest that a direct effect of the diuretics on oxidative metabolism in renal cells took place. Alteration in the activity of Na+-K+-ATPase was observed only in vivo and in those nephron sections, where sodium reabsorption was decreased under the effect of furosemide.

Adenosine Triphosphatases↗
PubMed1975

Metabolism of isolated kidney tubules. Independent actions of catecholamines on renal cyclic adenosine 3':5'-monophosphate levels and gluconeogenesis.

Isolated kidney cortex tubules from starved rats have been used to study the actions of catecholamines on renal adenosine 3':5' monophosphate (Ado-3':5'-P) levels and gluconeogenesis. In accordance with previous workers, norepinephrine was found to increase glucose formation from lactate and pyruvate and to a smaller degree from malate, succinate, fumarate and glutamine. The stimulatory effect of 0.5 muM norepinephrine was additive to that of 0.1 mM Ado-3':5-P, indicating an Ado-3':5'-P-independent mechanism of catecholamine action. The effects of parathyroid hormone and oleate on gluconeogenesis were also additive to that of norepinephrine. A comparative study of the actions of different catecholamine derivatives revealed that gluconeogenesis was stimulated in parallel to the alpha-adrenergic potency of the hormones, whereas Ado-3':5'-P levels were increased according to the known beta-stimulatory potency of the agents. Although isoproterenol was by far the most effective in raising Ado-3':5'-P levels, it was without effect on glucose formation from pyruvate, when added at 0.1 muM. At the same concentration, phenylephrine, which had no effect on Ado-3':5'-P levels, was the best stimulator of gluconeogenesis. The alpha-receptor blocking agent phentolamine inhibited the stimulatory effect of catecholamines on gluconeogenesis with a 50 times higher potency than propranolol, a beta-blocking agent. The fact that the stimulatory effect of Ado-3':5'-P was also blocked by propranolol, indicated an unspecific mechanism of action of this substance. The results indicate that the stimulatory effect of catecholamines on renal gluconeogenesis are mediated by an alpha-receptor and that they are independent from the stimulation of renal adenyl cyclase by these agents.

Animals↗
PubMed1979

Kidney tubule basement membrane alterations in type II membranoproliferative glomerulonephritis.

Fourteen kidney biopsy specimens from nine patients with type II membranoproliferative glomerulonephritis (MPGN) were examined by electron microscopy for tubular basement membrane (TBM) alterations. In all biopsies, laminal densities, charateristic for type II MPGN, were present in the glomerular basement membranes. The TBM alterations observed included: 1) the presence of laminal, and/or discrete, and/or aggregated densities; 2)focal thickening; 3) multilamination; and, 4) vesicular structures. Laminal densities occurred in 6 of the 9 cases examined. All biopsies had TBM densities representative of at least one of the three forms. The occurrence of electron densities in or near the TBM in type II MPGN may have diagnostic value. In those biopsies where tissue is insufficient for immunofluorescence microscopy and where glomeruli are not found on electron microscopy, an electron microscopic search for densities associated with TBMs would be warranted. Although TBM-associated densities are not pathognomonic for type II MPGN, the observation of such densities, espically laminal densities, would be useful in complementing light miccrscopic and clinical findings.

Adolescent↗