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K Thurau

Publications and source records attributed to K Thurau.

At least 37 records · Page 2Linked to original sources
PubMed1996

Heat shock proteins HSP25, HSP60, HSP72, HSP73 in isoosmotic cortex and hyperosmotic medulla of rat kidney.

The distribution of heat shock proteins (HSP) HSP60, HSP73, HSP72 and HSP25 in the isoosmotic cortex and the hyperosmotic medulla of the rat kidney was investigated using Western blot analysis and immunohistochemistry. HSP73 was homogeneously distributed throughout the whole kidney. The level of HSP60 was high in the renal cortex and low in the medulla. HSP25 and HSP72 were present in large amounts in the medulla. Only low levels of HSP25 and almost undetectable amounts of HSP72 were found in the cortex. HSP25 exists in one nonphosphorylated and several phosphorylated isoforms. Western blot analysis preceded by isoelectric focussing showed that HSP25 predominates in its nonphosphorylated form in the outer medulla but in its phosphorylated form in cortex and inner medulla. Although this intrarenal distribution pattern was not changed during prolonged anaesthesia (thiobutabarbital sodium), a shift from the nonphosphorylated to the phosphorylated isoforms of HSP25 occurred in the medulla. The characteristic intrarenal distribution of the constitutively expressed HSPs (HSP73, HSP60, HSP25) may reflect different states of metabolic activity in the isoosmotic (cortex) and hyperosmotic (medulla) zones of the kidney. The high content of inducible HSP72 in the medulla most likely is a consequence of the osmotic stress imposed upon the cells by the high urea and salt concentrations in the hyperosmotic medullary environment.

Anesthetics↗
PubMed1996

A transient role of the kidney in the maintenance of hypertension.

Using the Prague hypertensive rat (PHR), a model derived from the Wistar rat, in which a normotensive parallel, the Prague normotensive rat (PNR), was bred from the same parent pair (so that transplantation of organs between both these parallel rat model lines results in no distinct signs of rejection), we were able to show that hypertension travels with the kidney. Transplantation of a kidney from PHR to a bilaterally nephrectomized (BNX) PNR led to an increase in systolic blood pressure (SBP) in the recipient for 10 weeks after grafting. Similarly, a decrease in SBP was seen in BNX PHR for the same period of time after grafting a kidney from PNR. If, however, the SBP was measured over a longer period of time, because the elevated SBP slowly drops after grafting a kidney from PHR to BNX PNR, it is less than 130 mm Hg in the fourth month and thereafter. If BNX PHR receives a kidney from PNR, the decrease in SBP is permanent, amounting to 126.3 +/- 12.7 mm Hg one year after transplantation. The grafting of a heart from PHR to the abdominal aorta of PNR does not influence SBP. In conclusion, the presence of a kidney from PHR is necessary for the development, but is not sufficient for the maintenance of hypertension. The heart of PHR is not "hypertensogenic" as is the kidney.

Animals↗
PubMed1996

Ketoconazole inhibits organic osmolyte efflux and induces heat shock proteins in rat renal medulla.

Although ketoconazole (KC) is known to inhibit the cellular efflux of organic osmolytes in vitro, it is not known whether this effect can also be shown in vivo. Inhibition of osmolyte efflux by KC would impair osmotic adaptation and result in stress to the cells of the renal medulla when extracellular osmolality falls. Stress-inducible heat shock proteins (HSPs) may also participate in this response to osmotic stress. The aim of the present study was thus to establish whether KC inhibits organic osmolyte efflux from the cells of the renal medulla in vivo in response to a furosemide diuresis, and to establish whether HSPs are involved. A 20-minute furosemide infusion reduced urine osmolality and medullary urea content in control and KC-treated rats similarly. However, the efflux of methylamines (glycerophosphorylcholine, betaine) and polyols (myo-inositol, sorbitol) was attenuated in KC-treated rats while the efflux of amino acids was not significantly affected. Phosphorylation of HSP25 after the 20-minute furosemide diuresis was increased in KC rats. With continuing diuresis this returned to control levels after three hours. While short-term (up to 3 hr) diuresis did not alter the absolute amounts of HSPs in the renal medulla, long-term (24 or 48 hr) diuresis was associated with significantly increased amounts of HSP25 and HSP72 in KC-treated rats compared with control. These results suggest that KC inhibits the efflux of methylamines and polyols, thus impeding osmoadaptation of renal medullary cells during the onset of diuresis. This situation apparently increases the osmotic stress experienced by the cells of the renal medulla and provokes expression of HSP25 and HSP72.

Animals↗
PubMed1996

Carl Friedrich Wilhelm Ludwig: the founder of modern renal physiology.

The revolutionary "Zeitgeist" in the Europe of the 1840s left its mark no less in science than it did in the social and political life of the population. The essence of the scientific revolution was the change in paradigm from a vitalist-inductive to a mechanistic hypothetico-deductive approach, in which the experiment assumed the central role. The initiator of this new approach was a young physiologist in Marburg, Germany-Carl Friedrich Wilhelm Ludwig- and the first document his 1842 Habilitation thesis. Although this thesis was limited to a study on renal function, the impact of this epochal new approach, namely the analysis and explanation of living phenomena solely on the basis of physics and chemistry, went far beyond renal physiology: it revolutionised thinking in all the biological sciences. In this thesis, Carl Ludwig enunciated the principle of glomerular ultrafiltration driven by physical forces alone, i.e., the difference in the hydrostatic and oncotic pressures of the blood in the glomerular capillaries, a concept which remains valid today. Ludwig thus became the first scientist to describe correctly a principal component of renal function, the process of glomerular filtration.

Europe↗
PubMed1995

Ischemia-induced changes in cell element composition and osmolyte contents of outer medulla.

The effect of 60 minutes of ischemia and subsequent reflow on cell electrolyte and water homeostasis in the rat renal outer medulla was studied by determining sodium, potassium, chloride and phosphorus concentrations and dry weights in individual tubule cells using electron microprobe analysis. HPLC was employed to measure glycerophosphorylcholine, betaine, inositol and sorbitol, as well as several free amino acids in cortical and outer medullary tissue. Ischemia caused cell sodium and chloride concentrations to rise and cell potassium and phosphorus concentrations and cell dry weights to fall. These changes were most pronounced in the proximal straight tubule (PST) cells, less in thick ascending limb (MAL) and outer medullary collecting duct (OMCD) dark cells and barely noticeable in OMCD light cells. Except for some PST cells these changes were almost completely reversed 60 minutes after reintroducing blood flow. After 24 hours of reperfusion the number of PST cells exhibiting deranged electrolyte homeostasis was greatly increased. The contents of glycerophosphorylcholine, betaine or inositol in the cortex and outer medulla were not affected immediately following ischemia. After 24 hours of reperfusion, the cortical contents of osmolytes were still normal, while outer medullary contents were reduced. Except for low glycine contents, the ischemia-induced changes in amino acid contents were reversed after 24 hours of reflow in the cortex, whereas in the outer medulla aspartate, glycine and taurine contents were diminished. These results indicate increasing manifestation of PST cell injury in the reflow period. The defective re-accumulation of organic osmolytes and free amino acids in the outer medulla during reflow may reflect reduced interstitial tonicities, or may be due to inappropriate cellular uptake, synthesis or/and release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Restoration of urine concentrating ability and accumulation of medullary osmolytes after chronic diuresis.

Restoration of urine osmolality (Uosm) and medullary osmolyte contents after chronic diuresis was studied in rats infused for 6 days with furosemide and subsequently given the vasopressin analogue, 1-desamino-8-D-arginine vasopressin (DDAVP). Papillary tip intra- and extracellular electrolyte concentrations were measured by electron microprobe analysis, tissue contents of methylamines (glycerophosphorylcholine, betaine), polyols (myo-inositol, sorbitol), and several amino acids in different kidney zones by high-performance liquid chromatography. Administering DDAVP continuously after diuresis increased Uosm from (means +/- SE) 348 +/- 8 to 1,265 +/- 127 after 1 day and 2,485 +/- 186 mosmol/kgH2O after 3 days. The sum of all osmolytes at the papillary tip rose from 309.2 +/- 28.9 to 690.9 +/- 105.8 and 1,282.8 +/- 21.0 mmol/kg protein after days 1 and 3, respectively. Although interstitial tonicity (sum of Na, Cl, and K concentrations) was increased by 116 and 223% after 1 and 3 days DDAVP, intracellular tonicity was similar in chronic diuresis and following 1 or 3 days DDAVP. Coadministration of DDAVP with betaine, myo-inositol, and choline ("osmolyte treatment") did not accelerate the restoration of Uosm but caused significantly higher contents of osmolytes (except myo-inositol) in inner medulla and/or papilla after 3 days. In a minority of animals, restoration of Uosm and reaccumulation of medullary osmolytes were impeded in both DDAVP- and DDAVP/osmolyte-treated rats. These data indicate that, after chronic diuresis, accumulation of organic osmolytes and restoration of Uosm proceed in parallel. Capacity for transport and/or synthesis of organic osmolytes, rather than their availability, appear to limit reaccumulation on the first day of recovery. By the third day, delivery of some osmolytes or their precursors may limit the restoration of medullary osmolyte content. The failure of some rats to attain sufficient concentrating ability within this time period may be related to deficient reaccumulation of medullary osmolytes.

Amino Acids↗
PubMed1995

Effect of lesions to the supramammillary area of the posterior hypothalamus on atrial natriuretic peptide release following acute blood volume expansion in conscious Wistar rats.

Acute blood volume expansion (AVE) is a potent stimulus for atrial natriuretic peptide (ANP) release. Since several central nervous structures are well known for their involvement in the regulation of fluid and electrolyte homeostasis and in the secretion of central ANP, we carried our experiments on 33 conscious Wistar rats in order to determine if the integrity of the supramammillary (SMA) hypothalamic area is essential for the peripheral ANP response to AVE. We performed stereotaxic electrolytic lesions of SMA in part of the animals. To obtain AVE we administered 2 mL saline/100 g b.m. for 2 minutes into v. jugularis through the chronically implanted venous catheters. Plasma ANP was assayed radioimmunologically. AVE significantly increased plasma ANP both in the intact animals and in the lesioned rats. This concluded that SMA is not involved in the regulation of peripheral ANP release during AVE.

Animals↗
PubMed1994

Modulation of plasma arginine vasopressin during rehydration in the Bedouin goat.

When severely dehydrated Bedouin goats were allowed to drink to satiation their plasma arginine vasopressin concentration immediately dropped from a value of 19.9 +/- 9.4 pmol.l-1 to 9.4 +/- 3.9 pmol.l-1 (P < 0.05). It continued to drop further until a concentration of 1.8 +/- 2.9 pmol.l-1 was recorded, similar to that reported for goats allowed to drink freely. When the goats were shown the water but drinking was denied, plasma arginine vasopressin immediately dropped to 11.7 +/- 4.0 pmol.l-1 (P < 0.05) and further decreased to 10.0 +/- 4.8 pmol.l-1 5 min following their sighting the water. This level, however, was not sustained and 2 h after the initial drop the high pre-trial concentration of plasma arginine vasopressin was regained. Presumably, sighting of water by dehydrated goats induces an abrupt drop in their plasma arginine vasopressin level even before drinking commences. When rehydrated, by introducing water directly to the rumen, circumventing both the sensing of the water and the drinking proper, no immediate drop in the plasma arginine vasopressin concentration of the newly rehydrated goats was observed. A delayed drop in the plasma arginine vasopressin levels took place slowly, concurrently with the drop in osmolality and concentration of Na+ in the plasma. It is suggested that sighting of water by dehydrated goats is involved in the modulation of plasma arginine vasopressin.

Animals↗
PubMed1994

Loop diuretics affect transcellular electrolyte transport in cells of the distal convoluted tubule.

Although loop diuretics act preferentially on sodium chloride absorption in the thick ascending limb of the loop of Henle in the nephron, high concentrations of some loop diuretics also impair sodium absorption in the distal convoluted tubule (DCT). To characterize further the inhibitory effect of these agents on sodium absorption in the DCT, the action of torsemide and furosemide on cell sodium, chloride and potassium concentrations was examined in individual DCT cells of the kidney cortex and also, for comparison, in proximal convoluted tubule cells. In addition, initial cell uptake rates of rubidium, an index of in vivo Na+/K(+)-ATPase activity, were studied. Both diuretics caused a significant reduction of intracellular sodium concentration and rubidium uptake in DCT cells but not in connecting tubule, principal, intercalated or proximal tubule cells. These findings are consistent with the concept that both diuretics reduce transcellular sodium absorption in DCT cells by impairing sodium entry across the apical cell membrane and, as a consequence, sodium extrusion by primary active Na+/K+ (Rb+) exchange across the basolateral membrane.

Animals↗
PubMed1994

Atrial natriuretic peptide and dopamine in a dog model of acute renal ischemia.

Atrial natriuretic peptide (ANP) has been shown to reverse functional impairment in ischemic acute renal failure (ARF). To prolong and/or to enhance the effects of peptide, in this investigation dopamine (D) (3 micrograms/kg BW/min) was applied together with ANP (100 ng/kg BW/min) after 90 min unilateral renal artery occlusion in anesthetized dogs. ANP significantly increased creatine clearance, filtration fraction, diuresis, sodium excretion, sodium reabsorption, and free water clearance, as in postinfusion period only V remained elevated. D alone did not effect renal function beneficially. ANP+D improved kidney function impairment to a level comparable with that of ANP alone, but V and UNa.V remained increased in the postinfusion period. MAP was elevated during ANP+D infusion as compared to ANP alone and was sustained to the end of the experiment. We conclude that D does not potentiate the positive effects of ANP on postischemic kidney, but prolongs its action on UNa.V, possibly by maintenance of high MAP after renal ischemia.

Acute Kidney Injury↗
PubMed1993

The role of the kidney in the development of hypertension: a transplantation study in the Prague hypertensive rat.

It has been shown that genetic hypertension in rats usually "travels with the kidney". To elucidate the mechanism of this phenomenon further, experiments were carried out in the Prague hypertensive (PH) rat, a model of genetic hypertension derived from the Wistar strain, in which a normotensive parallel, the Prague normotensive (PN) rat, was also bred from the same parent pair. Thus, it is possible to transfer organs between both parallels without substantial signs of rejection and without the use of immunosuppressive drugs. Unilateral nephrectomy and transplantation of one kidney between PH and PN rats, did not affect the arterial blood pressure (BP). Transplantation of one kidney from PN rats to bilaterally nephrectomised PH rats normalised the high BP. If a PH rat was left with one original kidney in situ after the transplantation of a "normotensive" kidney, the high BP persisted until the original "hypertensive" kidney was removed. This removal resulted in sustained normalisation of BP. When the development of high BP in the PH rats was prevented for 2 months after weaning by antihypertensive drugs, transplantation of kidneys from these rats to bilaterally nephrectomised PN rats always induced a sustained hypertension in the recipient. These results argue against a role of high-BP-induced damage to the kidney and against an intrinsic increase in the salt-reabsorptive capacity of the tubular epithelium in PH rats. The data support the view that the kidney from PH rats produces a "hypertensinogenic" substance, the secretion of which is genetically determined and is not influenced by the magnitude of the BP.

Animals↗
PubMed1993

Transcellular sodium transport and basolateral rubidium uptake in the isolated perfused cortical collecting duct.

The relation between transcellular Na+ absorption, intracellular Na+ concentration and Na+/K(+)-ATPase activity (the last estimated by the rubidium uptake across the basolateral cell membrane) was examined in the different cell types of the rabbit cortical collecting duct (CCD). Experiments were performed on isolated perfused CCD in which Na+ absorption was varied by perfusing the tubule with solutions containing different Na+ concentrations (nominally Na(+)-free, 30 mM and 144 mM). Experiments were terminated by shock-freezing the tubules during perfusion. Precisely 30 s before shock-freezing, the K+ in the bathing solution was exchanged for Rb+. Intracellular element concentrations, including Rb+, were determined in freeze-dried cryosections of the tubules using energy-dispersive X-ray analysis. Increasing Na+ concentration in the perfusion solution caused significant rises in intracellular Na+ concentration and Rb+ uptake of principal cells. Principal cell Na+ and Rb+ concentrations were 7.8 +/- 0.9 and 7.0 +/- 0.8 mmol/kg wet weight respectively, when the perfusion solution was Na(+)-free, 10.1 +/- 0.7 and 11.6 +/- 0.6 mmol/kg wet weight with 30 mM Na+ in the perfusion solution, and 14.5 +/- 1.5 and 14.9 +/- 0.9 mmol/kg wet weight with 144 mM Na+ in the perfusion solution. In contrast, a comparable relationship between lumen Na+ concentration, intracellular Na+ concentration and basolateral Rb+ uptake was not seen in intercalated cells. These results support the notion that principal, but not intercalated, cells are involved in transepithelial Na+ absorption. In addition, the data demonstrate that apical Na+ entry and basolateral Na+/K(+)-ATPase activity are closely coupled in principal cells of the rabbit CCD.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1993

Osmotic adaptation of renal medullary cells during transition from chronic diuresis to antidiuresis.

The cells of the renal medulla adapt osmotically to high extracellular tonicities by high concentrations of organic osmolytes. Intracellular accumulation of these substances is, however, relatively slow. The aim of the present study was to assess the effect of an abrupt rise in extracellular tonicity on intracellular osmotically active substances after prior reduction of medullary contents of organic osmolytes by chronic diuresis. Intra- and extracellular electrolyte concentrations at the papillary tip and the tissue contents of methylamines (glycerophosphorylcholine, betaine), polyols (myo-inositol, sorbitol), and several amino acids were determined in the different kidney zones by electron microprobe analysis and high-performance liquid chromatography in control animals, in rats infused for 6 days with furosemide via osmotic minipumps, and in rats given the vasopressin analogue [deamino-Cys1,D-Arg8]vasopressin (DDAVP) after the chronic furosemide treatment. Chronic diuresis greatly reduced interstitial tonicity and inner medullary contents of methylamines and polyols and moderately reduced inner medullary amino acid contents but did not significantly affect intracellular electrolyte concentrations. When the diuretic rats were infused with DDAVP for 2 h, interstitial tonicity more than doubled and intracellular K and Cl concentrations rose by approximately 60 and 160%, while inner medullary contents of methylamines, polyols, and amino acids were not changed significantly. These data demonstrate that after effective depletion of medullary organic osmolytes by long-term diuresis, the cells of the renal papilla adapt osmotically to an abrupt increase in extracellular tonicities by elevated cell electrolyte concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
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↗