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Biomedical subjects

K Thurau

Publications and source records attributed to K Thurau.

At least 19 recordsLinked to original sources
PubMed1992

Effect of increased distal sodium delivery on organic osmolytes and cell electrolytes in the renal outer medulla.

Sodium absorption in distal tubule segments was stimulated by increasing the distal delivery via infusion of hypertonic saline. In these animals, and in control rats, electrolyte concentrations in thick ascending limb cells, light and dark cells of the collecting duct in the outer and inner stripe of the outer medulla and in cells of the proximal straight tubule (outer stripe only) were studied. The measurements were performed by electron microprobe analysis of freeze-dried cryosections of the outer medulla. In addition, organic osmolytes (glycerophosphorylcholine, betaine and myo-inositol) were measured by high performance liquid chromatography in cortex and outer medulla. Augmented delivery of sodium chloride to the distal tubule was associated with increased sodium concentrations of thick ascending limb cells both in the outer and inner stripe and of medullary collecting duct light and dark cells in the outer stripe. While the sum of organic osmolyte concentrations was 28% higher in the outer medulla of the salt-loaded animals compared with controls, this value was unchanged in the renal cortex. These findings indicate that the primary event underlying stimulation of sodium absorption along the thick ascending limb during increased distal sodium delivery is enhanced entry of sodium across the apical cell membrane. This would be expected to lead to higher cell sodium concentrations and stimulation of basolateral active Na-K-exchange. The enhanced transport activity of outer medullary tubules may be associated with increased interstitial tonicities and intracellular retention of organic osmolytes.

Animals↗
PubMed1992

Effect of K depletion on renal K and Rb excretion: evidence for activation of K reabsorption.

Prolonged potassium depletion activates tubular transport mechanisms mediating potassium absorption. To study ion specificity and factors that modulate the activity of potassium transport pathways, fractional potassium excretion (FEK) was compared with that of rubidium (FERb) in control and potassium-depleted rats subjected to various experimental maneuvers. In control rats FEK considerably surpassed FERb (FEK/FERb 1.54 +/- 0.08; mean +/- SEM), whereas in potassium-depleted rats FEK was significantly lower than FERb (FEK/FERb 0.72 +/- 0.05). Preferential retention of potassium compared to rubidium in potassium-depleted rats was accentuated (FEK/FERb 0.33 +/- 0.01) when residual potassium secretion was inhibited by amiloride and K-H exchange stimulated by increased distal buffer delivery (metabolic alkalosis). When distal fluid and buffer delivery were increased in control animals by acetazolamide, FEK and FERb rose in parallel. In potassium-depleted rats only FERb but not FEK was enhanced by acetazolamide. These data demonstrate that both potassium secretory and potassium absorptive transport pathways prefer potassium to its congener rubidium. Prolonged potassium depletion activates a potassium absorptive mechanism which is stimulated by increased distal buffer delivery and which transports potassium more effectively than rubidium.

Absorption↗
PubMed1992

Effect of loop diuretics on organic osmolytes and cell electrolytes in the renal outer medulla.

Electron microprobe analysis on freeze-dried cryosections was used to determine the effect of the loop diuretics torasemide and furosemide on intracellular electrolyte concentrations in individual cells of the outer and inner stripe of the outer medulla and on cell rubidium uptake, the latter a measure of basolateral Na-K-ATPase activity. In addition, the organic osmolytes glycerophosphorylcholine (GPC), betaine, inositol and sorbitol in cortex, outer medulla and inner medulla were measured using HPLC. Both loop diuretics significantly reduced sodium and chloride concentrations and rubidium uptake in thick ascending limb cells, but did not affect sodium concentration or rubidium uptake in the proximal straight tubule (PST) cells or in the light or dark cells of the outer medullary collecting duct (OMCD). Chloride concentrations in these cells (that is, PST cells, OMCD light and dark cells) were lowered by loop diuretics, albeit less than in thick ascending limb cells. Administration of both loop diuretics for only 20 minutes was sufficient to significantly depress tissue concentrations of GPC, betaine, and myo-inositol in the outer medulla and of GPC, betaine and sorbitol at the papillary tip. These results indicate that loop diuretics, presumably by blocking apical sodium entry, decrease thick ascending limb cellular sodium concentration and, as a consequence, reduce Na-K-ATPase activity as assessed by cell rubidium uptake. Although this has been shown previously in in vitro preparations, the present study confirms this for the first time in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Osmolytes in renal medulla during rapid changes in papillary tonicity.

The effect of acute changes in extracellular tonicity on cell electrolyte concentrations at the renal papillary tip and on organic osmolytes in different kidney zones was studied using electron microprobe analysis and high-performance liquid chromatography in four groups of rats: controls, 1- or 4-h water diuresis, and 4-h water diuresis followed by 30-min deamino-[Cys1,D-Arg8]vasopressin (ddAVP). The sum of the papillary interstitial concentrations of Na, K, and Cl was reduced from 981 mmol/kg wet wt in controls to 318 mmol/kg wet wt after 4-h diuresis and increased after ddAVP to 840 mmol/kg wet wt. In papillary collecting ducts intracellular electrolytes fell from 225 to 156 mmol/kg wet wt after 4-h diuresis and rose to 268 mmol/kg wet wt (significantly higher than control) after ddAVP. Organic osmolytes [sum of glycerophosphorylcholine (GPC), betaine, myo-inositol, and sorbitol] at the papillary tip decreased from 2,018 (control) to 1,037 mmol/kg protein after 4-h diuresis and did not increase after ddAVP. After ddAVP, cell P concentration, an index of cell GPC concentration, increased, indicating cell shrinkage. GPC concentration increased, indicating cell shrinkage. The results suggest that the concentrations of all osmoeffectors in papillary cells initially increase due to cell shrinkage in response to hypertonic stress. The higher intracellular ionic strength may be a signal for modulation of transport and metabolism of organic osmolytes.

Animals↗
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↗