Publications by authors named "Oberleithner H"

Studies were performed to investigate potassium transport in early distal tubule of the doubly-perfused kidney of Amphiuma under control conditions and following K-adaptation. Double barreled K-sensitive microelectrodes were used in stationary microperfusion experiments. Net K-flux was evaluated along with measurements of both cell membrane potential and cell K activity.

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From previous studies it is known that a furosemide-sensitive sodium chloride cotransport system is operative in the luminal cell membrane of the early distal amphibian tubule. Since inhibition of sodium chloride cotransport prevents potassium reabsorption in this nephron segment, experiments were carried out to evaluate further the possible relationship between sodium chloride and potassium transport by studying the changes of cellular sodium activity following luminal deletion of potassium ions. Sodium-sensitive liquid ion exchange microelectrodes and conventional microelectrodes were employed to determine the transepithelial potential (PDte), the peritubular cell membrane potential (PDpt) and the intracellular sodium activity (Nai+) in the presence and absence of luminal potassium.

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Previous experiments in the early distal tubule of the doubly perfused kidney of Amphiuma demonstrated net reabsorption of potassium (K) which is reversed to net K secretion after K adaptation. Furthermore, it is known that this particular segment exhibits extensive chloride (Cl) net reabsorption which depends on the presence of sodium (Na) and which is inhibited by furosemide. In order to test for a possible interrelationship between NaCl and K transport, K activity in lumen and cell, transepithelial electrical potential difference, peritubular cell membrane potentials and volume reabsorption were measured in control animals and after K adaptation, in presence and absence of furosemide.

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Correlation of ionized calcium concentration, [Ca2+] and blood pH has long been recognized. So far no distinction of the acid-base changes, i.e.

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The present study was designed to define the prerequisites of carbonic anhydrase independent bicarbonate reabsorption. In free flow experiments during systemic application of carbonic anhydrase inhibitor benzolamide (50 mg/kg B. W.

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Experiments were performed in the distal tubule of the doubly-perfused kidney of Amphiuma to determine active and passive forces, involved in the transport processes of potassium, sodium and chloride. Ion-sensitive microelectrodes and conventional microelectrodes were applied to estimate intracellular ion activities, cell membrane potentials and net flux of potassium and chloride under control conditions and during inhibition of active transport. Sodium chloride cotransport, located in the luminal cell membrane is postulated, based on the following observations: Total omission of sodium from the tubular lumen inhibits furosemide sensitive chloride reabsorption, decreases the lumen positive transepithelial potential difference and leads to a dramatic decrease of intracellular chloride.

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Previous experiments had demonstrated that cell chloride activities in early distal tubule cells of Amphiuma are above equilibrium distribution. Chloride activities fell sharply towards electrochemical equilibrium following perfusion of the tubular lumen with furosemide or with sodium-free solutions. These results suggested a furosemide-sensitive sodium chloride cotransport system in the luminal cell membrane.

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To characterize the mechanism of chloride transport across individual cell membranes, experiments were carried out on early distal tubules in the doubly perfused Amphiuma kidney and net chloride flux, transepithelial and transmembrane cell potentials, and intracellular chloride activity measured. Net chloride flux was evaluated by a modified stationary microperfusion technique, and intracellular and intraluminal chloride activities by means of double-barreled liquid ion exchange microelectrodes. Control conditions were characterized by significant net volume and chloride reabsorption, a transepithelial potential difference of +9.

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Since bicarbonate has been reported to elicit fast recovery from acute renal failure in man, clearance studies were performed to compare the effects of sodium bicarbonate and saline infusion on renal function in postischaemic renal failure in the rat. In a first set of experiments the left kidney and in a second both kidneys were clamped for a period of 45 min and renal function monitored up to 210 min after release of the clamp. Glomerular filtration rate (ml/min) decreased following clamping from (mean values +/- SEM) 1.

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To differentiate between extrarenal and renal causes of hyperuricaemia and gout, clearances of urate and creatinine were monitored for 3 1/2 days in fifty-two individuals (seven with a history of gout) with no gross impairment of renal function (creatinine clearance 52-137 ml/min). Dietary purine intake was kept constant. Monophasic circadian fluctuations of fractional urate excretion (= urate clearance over creatinine clearance) were observed with peak values in the afternoon, about 50% higher than during the night.

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Parathyrin and calcitonin exert their effects on phosphate metabolism by influencing the functions of at least three organ systems, i. e. bone, gut and kidneys.

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A new system for continuous in vivo measurement of ionized calcium in blood is presented. The system consists of a small chamber (400 microliter) which is thermostatized at 37 degrees C and contains a glass electrode for pH measurement and a calcium selective electrode. The chamber is mounted in an arteriovenous shunt between the femoral artery and femoral vein of heparinized (approximately 1IU/min.

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Both urate and oxalate are organic acids of considerable clinical interest, owing to their limited solubility. Calcium oxalate is the most frequent constituent of renal calculi and occasionally precipitates in body fluids. Urate precipitations are common in the kidney and in various other tissues.

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In previous studies it has been demonstrated that a decline of plasma calcium concentration accounts for the decrease of phosphate reabsorption in thyroparathyroidectomized (TPTX) rats undergoing phosphate loading. Microinfusion studies were performed in TPTX rats in order to discriminate between a systemic effect of calcium an a direct renal effect. Thyroparathyroidectomized animals were infused with a phosphate solution continuously.

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Luminal pH in early and late proximal tubules was recorded continuously with antimony microelectrodes before and during carbonic anhydrase inhibition. Following i.v.

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The site of outflux of 45Ca along the nephron were investigated using microinfusion technique in acutely thyroparathyroidectomized (TPTX), intact and TPTX Wistar rats substituted with parathyroid hormone (PTH). In all three groups 45Ca outflux occurred along the proximal tubule, the loop of Henle and along the distal tubule. After microinfusion into late distal tubules 45Ca recovery in ipsilateral urine was essentially complete for the TPTX group but was only 83 and 65% for the intact and the PTH substituted animals.

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Phosphate loading in acutely thyroparathyroidectomized rats is followed by a decline of phosphate reabsorption. In addition, a mixed respiratory and metabolic alkalosis and hypocalcemia develop. Normalization of plasma calcium concentration, unlike the reversal of the alkalosis, prevents the fall in phosphate reabsorption.

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