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Biomedical subjects

K Thurau

Publications and source records attributed to K Thurau.

At least 55 records · Page 3Linked to original sources
PubMed1992

Cellular changes in acute renal failure: functional and therapeutic consequences.

Prerenal, renal and postrenal forms of acute renal failure (ARF) are distinguishable. Prerenal forms are reversible by effective treatment of the underlying extrarenal disorder(s). Damage of the endothelium and the tubular epithelium indicates progress of prerenal to renal ARF or induction of primary renal ARF. A continuous survey of renal function based on the cellular and functional pathophysiologic pathways of ARF allows adequate and specific therapy. As both extra- and intrarenal causes of ARF may occur simultaneously under clinical conditions, a broad therapeutic approach should be used: treatment of the extrarenal disorder augmented by measures to reduce the cellular workload, cell-protective therapy, support of microcirculation rheology, and inhibition of prerenal vasoconstriction.

Acute Kidney Injury↗
PubMed1992

Intact kidney function during contralateral renal artery clamping in dogs.

Experiments were carried out on 32 Nembutal anaesthetized mongrel dogs from both sexes. After 45 min control period unilateral renal ischemia was achieved by clamping the left renal artery for 90 min. In part of the experiments (n = 8) after clamp removal 3 consecutive 45 min periods were performed. The function of the intact right kidney was investigated. Mean arterial pressure (MAP), heart rate (HR), glomerular filtration rate (GFR), urine flow rate (V), fractional excretions of sodium (FENa), potassium (FEK) and chloride (FECl) and plasma levels of atrial natriuretic peptide, dopamine and antidiuretic hormone were evaluated. During ischemia MAP was elevated from 122.5 +/- 3.1 to 140.2 +/- 2.7 mmHg (p < 0.001), HR decreased from 119 +/- 4 to 102.5 +/- 3.9 beats/min (p < 0.01) as compared to the control period. GFR did not change significantly, while all excretory parameters increased: V from 8.7 +/- 1.2 to 14.5 +/- 1.7 microliters/min/gr kidney tissue (p < 0.05); FENa from 2.3 +/- 0.2 to 3.6 +/- 0.3% (p < 0.01); FEK from 40.0 < 3.5 to 51.2 < 2.8% (p < 0.05); FECl from 1.8 < 0.3 to 2.6 < 0.3% (p < 0.05). MAP remained elevated in the first and the second postischemic periods and was paralleled by the sustained increase in FENa and FECl, while FEK remained higher to the end of the experiment. ANP was significantly elevated during ischemia: on 75 min--p < 0.01 and on 105 min.--p < 0.05. AVP and dopamine showed no statistically significant changes during the investigated periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Sodium entry routes in principal and intercalated cells of the isolated perfused cortical collecting duct.

Transmembrane sodium transport pathways were studied in principal and intercalated cells of the isolated perfused rabbit cortical collecting duct. Intracellular electrolyte concentrations in individual collecting duct cells were measured by electron microprobe analysis during blockage of basolateral Na-K-ATPase by ouabain and simultaneous inhibition of sodium entry across the apical and/or basolateral cell membrane. In principal cells the ouabain-induced rise in cell sodium concentration could only partially be blocked by amiloride (10(-4) mol/l) in the perfusion fluid. Amiloride (10(-3) mol/l) added to the bathing solution produced a further, significant reduction of sodium influx. In principal cells the ouabain-induced increase in sodium concentration was completely prevented by amiloride in the perfusion solution in combination with omission of sodium from the peritubular bathing solution. In intercalated cells ouabain caused a less pronounced increase in sodium concentration than in principal cells. Neither amiloride in the perfusate, nor amiloride in both bathing and perfusion solution, significantly reduced the ouabain-induced rise in intercalated cell sodium concentration. These results indicate that in principal cells amiloride-sensitive sodium channels constitute the predominant pathway for sodium entry across the apical cell membrane. In addition, substantial amounts of sodium enter principal cells across the basolateral cell membrane, probably via Na-H exchange. Finally, the data suggest that in intercalated cells sodium channels and the Na-H exchange are sparse or even absent.

Amiloride↗
PubMed1990

Effect of amiloride on electrolyte concentrations and rubidium uptake in principal and mitochondria-rich cells of frog skin.

The role of mitochondria-rich cells (MR cells) in transepithelial Na transport was investigated by determining electrolyte concentrations and Rb uptake in individual cells of frog skin epithelium using electron microprobe analysis. Measurements were performed under control conditions and after blocking the transepithelial Na transport with amiloride. Under control conditions, Na and Cl concentrations of MR cells scattered much more than those of principal cells and ranged from a few up to more than 30 mmol/kg wet weight. Rb uptake from the basal side into individual MR cells also showed a large variation and was, on the average, much less pronounced than into the principal cells. In principal cells, amiloride reduced the Na concentration and Rb accumulation. In contrast, no effect was observed upon electrolyte concentration and Rb uptake of MR cells. Rb uptake was correlated to the Na concentration of MR cells both under control conditions and after amiloride. It is concluded that, in contrast to the principal cells, MR cells are not involved in amiloride-sensitive transepithelial Na transport and that their Na/K-pump activity is very low.

Amiloride↗
PubMed1990

Effect of diuretics on cell potassium transport: an electron microprobe study.

To study the short-term uptake of potassium across the basolateral membrane into individual tubule cells, rubidium was used and measured by electron microprobe analysis. Changes of rubidium uptake were interpreted to reflect altered sodium entry and basolateral Na-K-ATPase activity. The effects of hydrochlorothiazide, amiloride and furosemide were determined in saline-loaded animals. Hydrochlorothiazide inhibited rubidium uptake in proximal convoluted and distal convoluted tubule cells. The effect was largest in distal convoluted tubule cells. Amiloride reduced rubidium uptake in principal cells as well as in proximal convoluted, distal convoluted and connecting tubule cells. Furosemide depressed rubidium uptake in distal convoluted tubule cells, but increased uptake in principal cells. Rubidium uptake into intercalated cells was not affected by any of the diuretics used. Hydrochlorothiazide and amiloride altered rubidium uptake also in cells not associated with the main diuretic action. These effects of hydrochlorothiazide and amiloride may be due to interference with cell transport mechanisms of Na-H and anion exchange.

Animals↗
PubMed1989

Localization of transport compartments in turtle urinary bladder.

To characterize different transport compartments in the urinary bladder epithelium of postabsorptive turtles, the electrolyte composition of individual cells was determined using electron microprobe analysis. After blocking the transepithelial Na transport, the short-circuit current decreased from positive to negative values (from 26.5 +/- 17.7 to -3.9 +/- 2.9 after ouabain and from 25.4 +/- 17.2 to -8.0 +/- 5.1 microA/cm2 after amiloride). Whereas under control conditions the Na and K concentrations were similar in all cell types and the same was true for Cl in most of the cells, some cells exhibited very low Cl concentrations. The epithelial cells were subdivided according to their electrolyte composition into ouabain-sensitive and ouabain-insensitive ones. In the ouabain-sensitive cells, which made up the majority of epithelial cells and showed a relatively high Cl concentration (about 36 mmol/kg wet weight), the Na concentration increased after ouabain by about 90 mmol/kg wet weight and the K concentration decreased by a similar amount. Since these alterations could largely be prevented when amiloride was applied before ouabain, it is suggested that the granular and basal cells form a syncytial Na transport compartment similar to that in other multilayered epithelia. The ouabain-insensitive cells, in which almost no alteration in Na and K concentrations was observed after ouabain, were subdivided into a Cl-rich (34.6 +/- 7.6 mmol/kg wet weight) and a Cl-poor (12.0 +/- 5.6 mmol/kg wet weight) population. Since in these cells no large mucin granules were detectable, they are regarded as carbonic anhydrase-rich cells involved in H and HCO3 transport.

Amiloride↗
PubMed1989

Effect of ouabain on electrolyte concentrations in principal and intercalated cells of the isolated perfused cortical collecting duct.

Sodium, phosphorus, chloride and potassium concentrations were measured by a new method in individual principal and intercalated cells in the cortical collecting duct in vitro. Electron microprobe analysis was applied to freeze-dried cryosections of the isolated perfused rabbit cortical collecting duct. Cell analyses were performed under control conditions and after addition of ouabain to the bath. Under control conditions similar sodium, potassium, chloride, and phosphorus concentration (means +/- SEM) were observed in principal (10.0 +/- 0.6, 126.5 +/- 2.7, 24.6 +/- 1.0, and 121.5 +/- 3.5 mmol/kg wet weight, respectively) and intercalated cells (9.0 +/- 0.9, 127.1 +/- 4.2, 27.4 +/- 1.8, and 118.7 +/- 4.9 mmol/kg wet weight, respectively). In principal cells ouabain (10 min) caused an increase in sodium and chloride concentrations by 104 and 13 mmol/kg wet weight, and a decrease in potassium and phosphorus concentrations by 106 and 32 mmol/kg wet weight. These changes in cell element concentrations can be ascribed to an exchange of intracellular potassium against extracellular sodium and to cell swelling due to influx of extracellular fluid. The effects of ouabain on intercalated cells were far less pronounced than on principal cells. This different susceptibility to ouabain of principal and intercalated cells can be ascribed to differences in active and passive transmembrane ion transport pathways.

Animals↗
PubMed1989

PGE2 concentrations in renal venous plasma and renal lymph during basal and stimulated conditions in the dog.

PGE2 concentration (pg/ml + SEM) was measured in canine renal lymph (394 +/- 115), renal venous plasma (276 +/- 55), arterial plasma (172 +/- 34) and urine (1290 +/- 934). Control periods were followed by an infusion of the sodium salt of arachidonic acid (AA) (40 micrograms/kg min) into the renal artery to stimulate prostaglandin synthesis. During infusion of AA PGE2 concentrations increased significantly in renal lymph (672 +/- 155) renal venous plasma (549 +/- 123), and urine (6768 +/- 1420), but not in the arterial plasma (176 +/- 31). Concentrations in renal lymph and renal venous plasma were not significantly different under either condition. These findings indicate that PGE2 concentration in renal venous plasma is, by and large, representative of mean PGE2 concentrations in the cortical renal interstitium, although focal inhomogeneities in PGE2 concentration in the different areas of the renal interstitium cannot be excluded. Since flow rate of renal lymph is insignificant in comparison with renal venous plasma flow rate total renal PGE2 output can be estimated from measurements in renal venous plasma and urine.

Animals↗
PubMed1989

Studies on the mechanism of rubidium-induced kaliuresis.

Renal clearance and electron microprobe methods were used 1) to elucidate the effects of chronic rubidium administration on potassium transport and 2) to localize, by the use of amiloride in acute experiments, the tubule site of interaction between rubidium and potassium. Substitution of drinking water by a 50 mM rubidium chloride solution for 9 to 11 days led to significant hypokalemia (plasma potassium 2.5 +/- 0.1 mM; plasma potassium plus rubidium 3.3 +/- 0.1 mM). Compared to a control group (reduction of plasma potassium to 3.4 +/- 0.1 mM by short-term potassium depletion) with a fractional potassium excretion of 2.1 +/- 0.3%, rubidium-treated rats excreted potassium at a much higher rate of 14.6 +/- 3.0%. The potassium content of principal cells was, however, significantly lower in rubidium-treated than in potassium-deprived animals. Similar to experiments in which rubidium was given acutely (3 hours), chronic rubidium administration was associated with preferential accumulation of rubidium in all tubule cells relative to potassium. Rubidium clearances were uniformly below those of potassium. Amiloride abolished the difference between rubidium and potassium clearances and sharply reduced the excretion of both cations. In view of the known site of action of amiloride, this suggests a distal tubule site of rubidium action on potassium transport. Amiloride also reduced or abolished the preferential uptake of rubidium into all but intercalated tubule cells. Marked cell heterogeneity of rubidium accumulation into intercalated cells was observed: One subpopulation, with low cell chloride, retained rubidium more effectively than another subpopulation with high cell chloride.

Amiloride↗
PubMed1988

Cellular osmoregulation in the renal papilla.

The cells of the renal papilla are subject to extreme variations in extracellular tonicity. To obtain more insight into the mechanisms whereby these cells adapt osmotically to these unique environmental conditions, elements were measured in individual cells of the rat renal papilla in antidiuresis and after prolonged furosemide administration. In antidiuresis cell sodium, chloride and potassium concentrations did not differ fundamentally from those observed in tubule cells exposed to isotonic surroundings such as in proximal tubule cells. The marked fall in extracellular electrolyte concentrations induced by furosemide was paralleled by a far less pronounced decline in intracellular sodium, chloride and potassium concentrations. These data indicate that papillary cells achieve osmoadaptation to widely differing extracellular tonicities mainly by varying the intracellular concentrations of osmotically active substances other than inorganic electrolytes. Since high concentrations of organic osmolytes (sorbitol, inositol, glycerophosphorylcholine and other trimethylamines) have been detected in the papilla and since the tissue contents of these compounds have been shown to vary in parallel with urine osmolality, it may be concluded that metabolically inert, organic osmolytes play a dominant role in the osmoregulation of renal papillary cells.

Animals↗
PubMed1988

Na transport compartment in rabbit urinary bladder.

Electron microprobe analysis was used to determine cellular electrolyte concentrations in rabbit urinary bladder. Under control conditions the mean cellular electrolyte concentrations were for Na 11.6 +/- 2.0, for K 124.1 +/- 15.3, and for Cl 26.0 +/- 5.1 mmol/kg wet weight. The dry weight content was 19.0 +/- 2.0 g/100 g. Inhibition of the Na/K-pump with ouabain resulted in drastic changes of the cellular element concentrations. Similar changes also occurred when in addition to ouabain the apical side was kept Na-free. In all epithelial layers the Na and Cl concentrations increased by 90 and 30 mmol/kg wet weight, whereas the K concentration and the dry weight content decreased by 90 mmol/kg wet weight and 6 g/100 g wet weight, respectively. With Na-free choline-Ringer's solution on the basal side ouabain led to a decrease in the K concentration by about 60 mmol/kg wet weight while the Na and Cl concentrations remained unchanged. These data indicate that the basolateral membrane is permeable to Na, choline, Cl, and K. Nystatin produced drastic changes in the cellular electrolyte concentrations when Na- or Rb-sulfate Ringer's solutions were present on the apical side. With Na-sulfate Ringer's solution the Na concentration increased by about 25, the Cl concentration by 30 mmol/kg wet weight and the dry weight content decreased by 4.5 g/100 g, respectively. With Rb-Ringer's solution about 20 mmol/kg wet weight of the cellular K was exchanged against Rb. The concentration changes were identical in all epithelial layers supporting the idea that the rabbit urinary bladder represents a functional syncytium with regard to the transepithelial Na transport.

Animals↗
PubMed1988

Na transport stimulation by novobiocin: intracellular ion concentrations and membrane potential.

Microelectrodes and electron microprobe analysis were employed to study the effect of novobiocin on membrane potential and intracellular electrolyte concentrations in the frog skin epithelium. In both species investigated (Rana esculenta and Rana temporaria), novobiocin (1 mM, outer bath) caused a stimulation of transepithelial Na transport, a depolarization of apical membrane potential, a fall in the apical fractional resistance, and an increase in the intracellular Na concentration. The rise in the Na concentration was accompanied by an equivalent fall in the K concentration. All effects of novobiocin were fully reversible by subsequent application of amiloride. The depolarization as well as the Na increase suggests that the natriferic effect of novobiocin is due to a stimulation of the apical Na influx. Combining both measurements it was possible to calculate the effect of novobiocin on the Na permeability of the apical membrane directly. In Rana esculenta novobiocin increased the permeability from 4.5 to 23.2 nm/s. In Rana temporaria the increase was significantly smaller, from 8.7 to 16.9 nm/s. The transport rate as measured by the short-circuit current showed a non-linear dependence on the apical Na permeability. In the range of transport rates normally encountered, however, the current was a linear function of the Na permeability consistent with the view that the apical membrane is rate-limiting in transepithelial Na transport.

Amiloride↗
PubMed1988

The distribution of potassium, sodium and chloride across the apical membrane of renal tubular cells: effect of acute metabolic alkalosis.

Studies were undertaken to define the effect of acute metabolic alkalosis (hypertonic sodium bicarbonate i.v.) on the chemical gradients for potassium, sodium and chloride across the apical membrane of individual renal tubule cells. Electron microprobe analysis was used on freeze-dried cryosections of the rat renal cortex to measure electrolyte concentrations in proximal tubule cells and in the various cell types of the superficial distal tubule. Analyses were also performed in fluid samples obtained by micropuncture from proximal and early and late distal collection sites. Compared with the appropriate controls (hypertonic sodium chloride i.v.), administration of sodium bicarbonate resulted only in small and mostly insignificant increases in cell potassium concentrations and induced only minor alterations in the cell/tubule fluid potassium concentration gradient for all cell types analysed. This observation suggests that under this condition factors other than an increase in cell potassium concentration are important in modulating potassium transfer across the apical membrane of potassium secreting cells. Nevertheless, since in alkalosis phosphorus and cell dry weight were decreased, and hence cell volume increased, in all but the intercalated cells, actually the potassium content of most tubular cells was higher under this condition. In comparison with animals infused with isotonic saline at low rates (hydropenic controls), infusion of either hypertonic sodium chloride or sodium bicarbonate led to a sharp increase in distal tubule fluid sodium concentrations and in the sodium concentrations of distal convoluted tubule, connecting tubule and principal cells, indicating that under both conditions the primary event causing enhanced transepithelial sodium absorption is stimulation of the sodium entry step.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkalosis↗
PubMed1988

Effect of acute metabolic acidosis on transmembrane electrolyte gradients in individual renal tubule cells.

We studied the effect of acute metabolic acidosis on potassium, sodium and chloride gradients across the apical membrane of proximal and distal tubule cells by determining electrolyte concentrations in individual cells and in tubule fluid employing electron microprobe analysis. Cellular measurements were performed on freeze-dried cryosections of the renal cortex, analysis of tubule fluid electrolyte concentrations on freeze-dried microdroplets of micropuncture samples obtained from proximal and from early and late distal collection sites. Acidosis (NH4Cl i.v. and i.g.) induced a substantial rise in plasma potassium concentration without significant effects on cell potassium concentrations. Potassium concentrations along the surface distal tubule were also unaltered; thus the chemical driving force for potassium exit from cell to lumen was not affected by acidosis. In all but intercalated cells acidosis markedly increased cell phosphorus concentration and cell dry weight indicating cell shrinkage and thus diminution of cell potassium content. Because the increase in intracellular chloride concentration exceeded the increase in plasma chloride concentration, the chemical chloride gradient across the contraluminal membrane was markedly depressed by acidosis.

Acidosis↗