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Biomedical subjects

F Lang

Publications and source records attributed to F Lang.

At least 451 records · Page 25Linked to original sources
PubMed1983

Interaction of intracellular electrolytes and tubular transport.

To disclose possible regulatory mechanisms, the potential difference across the peritubular cell membrane (PDpt) and intracellular activities of sodium (Nai+), potassium (Ki+), calcium (Cai2+), bicarbonate (HCO3i-) and chloride (Cli-) have been traced continuously during inhibition of Na+/K+-ATPase with ouabain. Within 31 +/- 4 min following application of ouabain, PDpt decreases (from 57 +/- 2 mV) to half and Ki+ by 37.7 +/- 2.2 mmol/l (from 63.5 +/- 1.9 mmol/l), Nai+ increases by 35.1 +/- 4.1 mmol/l (from 13.2 +/- 2.4 mmol/l), Cai2+ by 0.17 +/- 0.2 mumol/l (from 0.09 mumol/l), HCO3i-) by 3.0 +/- 1.1 mmol/l (from 15.3 +/- 2.0 mmol/l) and Cli- by 6.2 +/- 1.0 mmol/l (from 14.4 +/- 1.6 mmol/l). Within the same time the luminal and peritubular cell membrane resistances increase 45 +/- 15% and 53 +/- 17%, respectively. The increase of the resistances is mainly due to a decrease of K+ conductance, which in turn mainly accounts for the depolarisation of PDpt. Additional experiments demonstrate that the K+ conductance of the peritubular cell membrane is sensitive to the cell membrane potential difference and possibly linked to Na+/K+-ATPase activity. The decline of PDpt probably accounts for intracellular alkalinisation which in turn reduces Na+/H+ exchange. Na+-coupled transport of glucose and phenylalanine decrease in linear proportion to PDpt. The transport of these and probably of similar substances represents the main threat to electrolyte homeostasis of the cells.

Adenosine Triphosphatases↗
PubMed1983

The effect of cAMP on the cell membrane potential and intracellular ion activities in proximal tubule of Rana esculenta.

Experiments were performed in proximal tubule of the isolated perfused frog kidney to evaluate peritubular cell membrane potentials (PDpt), and the intracellular ion activities of sodium (Nai+), chloride (Cli-) and potassium (Ki+) under control conditions and following peritubular application of dibutyryl-cyclic AMP (cAMP, 2 X 10(-4) mol X 1(-1)). Conventional and ion-sensitive microelectrodes were applied to record continuously cAMP-induced changes of these parameters in individual proximal tubule cells. Within a few minutes a significant hyperpolarisation of PDpt (delta = 2.0 +/- 0.2 mV) occurs simultaneously with a decrease of Nai+ (delta = 2.5 +/- 0.5 mmol X 1(-1)). Ki+ increases (delta = 3.6 +/- 0.9 mmol X 1(-1)) and Cli- decreases (0.4 +/- 0.07 mmol X 1(-1)) slightly, but significantly. With both ions the alterations of the chemical gradient is significantly smaller than the potential shift. PDte is not significantly altered by cAMP. The cAMP-induced hyperpolarisation of PDpt can be observed in presence and absence of luminal glucose. However, omission of Na+ from the luminal perfusate abolishes the hyperpolarising effect of cAMP on PDpt. The results suggest that cAMP reduces sodium entry from the lumen into the cell, thus hyperpolarising the cell membrane and decreasing Nai+. Persistence of sensitivity of PDpt to cAMP after omission of glucose indicates that other Na+ coupled transport processes and/or passive Na+ conductance are affected by cAMP. the changes of Ki+ and Cli- are secondary, following the change of PDpt.

Animals↗
PubMed1983

Anthracene-9-carboxylic acid inhibits renal chloride reabsorption.

From previous studies, it is known that in the diluting segment, C1- -ions are transported from the tubule lumen into the cell together with Na+ and K+ via a furosemide-sensitive cotransport system. This carrier-mediated process, located in the luminal cell membrane, is driven by the steep "downhill" Na+ gradient (directed from lumen to cell) which is maintained by the ouabain-sensitive Na+/K+-pump at the peritubular cell membrane. C1- -ions are accumulated within the cell cytosol and are supposed to leave the cell by a C1- -conductive pathway. The present experiments, performed in diluting segments of the isolated perfused frog kidney, demonstrate the existence of a significant C1- -permeability of the peritubular cell membrane and its complete inhibition by anthracene-9-COOH. The data indicate that C1- -reabsorption can be reduced not only by the inhibition of luminal C1- -entry (i.e. by furosemide) but also by the blockade of the passive C1- -exit step across the peritubular cell membrane. Since complete inhibition of C1- -permeability reduces transepithelial uphill C1- -transport only to half, the data disclose the existence of an additional C1- -pathway at the peritubular cell membrane.

Animals↗
PubMed1983

Effect of luminal potassium on cellular sodium activity in the early distal tubule of Amphiuma kidney.

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. The ratio of the luminal cell membrane resistance over the peritubular cell membrane resistance (Rlu/Rpt) was also estimated. When potassium ions are omitted from the luminal perfusate, PDpt hyperpolarizes by some 20 mV, PDte approaches zero and Nai+ decreases by about 40%. Rlu/Rpt is more than doubled in the presence of a potassium-free perfusate. Both potential and resistance changes are fully reversible. Similar results were obtained in experiments in which Barium ions (1 mmol/1 BaCl2) were present during the luminal potassium substitution. Our results indicate that absence of potassium inhibits luminal sodium chloride entry; as a result of continued peritubular sodium extrusion cellular sodium activity falls. The increase of Rlu/Rpt following perfusion with a potassium-free perfusate is interpreted as a decrease of a significant electrodiffusive potassium conductance in the luminal cell membrane.

Animals↗
PubMed1983

Evidence for an amiloride sensitive Na+ pathway in the amphibian diluting segment induced by K+ adaptation.

The effect of amiloride on cell membrane potentials and intracellular Na activity (Nai) was tested in early distal tubules of the isolated perfused kidney of control and of K-adapted (high-K diet) Amphiuma. Conventional and Na-sensitive liquid ion-exchanger microelectrodes were employed to measure the peritubular cell membrane potential (PDpt), the transepithelial potential difference (PDte) and the Na electrochemical gradient across the peritubular cell membrane (ENapt), in the absence and the presence of amiloride (1 X 10(-4) mol X 1(-1] in both groups of animals. Amiloride did not affect PDpt and ENapt in control animals but depolarized PDpt and ENapt by about 8 mV in K-adapted animals. Nai (11.0 +/- 0.6 mmol X 1(-1) in early distal cells of control animals) did not change significantly by this maneuver. However, Nai decreased to extremely low values (2.3 +/- 0.2 mmol X 1(-1] when the luminal cotransport system for Na, Cl and K was inhibited by the luminal application of furosemide (5 X 10(-5) mol/l) and when the luminal cell membrane was exposed simultaneously to amiloride. The amiloride-induced effects on PDpt, ENapt and Nai occurred within seconds and were fully reversible. We conclude that high-K diet (K adaptation) induces an amiloride-sensitive pathway in the luminal cell membrane of early distal cells of Amphiuma which exists in parallel with the furosemide-sensitive cotransport system located in this cell barrier. The results suggest a luminal amiloride-sensitive Na/H exchange mechanism which regulates the luminal K permeability.

Adaptation, Physiological↗
PubMed1983

Receptors for insulin-like growth factors in rabbit articular and growth plate chondrocytes in culture.

Receptors for the insulin-like peptide ILAs have been identified in cultured rabbit chondrocytes. The cell-ILAs interaction is a time-dependent, reversible and saturable process. The cell-bound radioactive material appears as intact hormone. Insulin-like growth factor II (IGFII) is as potent as ILAs in competing for 125I-ILAs binding, whereas insulin-like growth factor I is somewhat less potent. Insulin does not affect ILAs binding. Our results suggest that the cultured chondrocytes possess a common receptor for the somatomedin peptides and that insulin, which is able to stimulate sulfate incorporation into proteoglycans, acts through an insulin receptor distinct from the somatomedin site. In growth plate chondrocytes the specific binding of 125I-ILAs is ten times lower than in articular cells in culture, whereas the sulfation activity of ILAs, at all concentrations studied, is 2.5-3 times lower in growth plate than in articular chondrocytes. The total binding of 125I-ILAs is higher to a particulate cell fraction than to intact cultured cells, by a factor of 10 for the growth plate cells, and by a factor of 2 for the articular cells. These findings suggest a poor accessibility of the hormone to the receptor sites of the growth plate chondrocytes in cultures, which are known to be surrounded by a thick matrix.

Animals↗
PubMed1982

[Horton's disease: retrospective study of 33 cases and review of the literature].

Temporal arteritis is still often overlooked in 1982 as shown by the diagnostic delay reported in a retrospective review of 33 patients and in the series previously published in the medical literature. Clinical features to be especially kept in mind are the occasional nature of temporal signs, the pathognomonic value of jaw claudication and the existence of signs which may constitute a premonitory syndrome of blindness. The frequent rise in alkaline phosphatase levels is often misleading. In patients over 65 with an unexplained inflammatory syndrome, biopsy of both temporal arteries should be promptly performed, prior to the unpleasant and costly investigations designed to detect an occult carcinoma. Corticosteroids are still the best treatment of giant cell arteritis but the optimal initial dosage remains unknown as no data from randomized trials are available. Symptomatic relapses have been reported up to 10 years (5 years for ocular symptoms) after onset of the disease. Because of this protracted course, which makes adequate follow-up difficult to ensure, recovery rates from different series are at variance. The main side-effects of maintenance corticosteroid therapy in these elderly patients are osteoporosis, which warrants systematic countermeasures, and probably an increased rate of atheromatosis.

Adrenal Cortex Hormones↗
PubMed1982

Carbonic anhydrase independent bicarbonate reabsorption.

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.) bicarbonate recovery in % of filtered load was found to be 74 +/- 8% in late proximal convoluted tubules, 39 +/- 6% in distal convoluted tubules and 32 +/- 4% in urine, indicating that most of carbonic anhydrase independent bicarbonate reabsorption occurs in tubule segments prior to distal convoluted tubules. In vivo continuous microperfusion experiments in proximal convoluted tubules demonstrated that luminal benzolamide (0.5 mmol/l) virtually abolishes net bicarbonate fluxes, when bicarbonate concentration in the luminal perfusate (25 mmol/l) is close to peritubular plasma concentration (24.4 mmol/l). In contrast, a significant downhill reabsorptive flux occurs, when perfusate bicarbonate concentration is 75 mmol/l and a significant downhill secretory flux is observed, when the perfusate is initially free of bicarbonate. The corresponding apparent permeabilities are 1.0 +/- 0.1 X 10(-6) cm2/s for influx and 1.6 +/- 0.4 X 10(-6) cm2/s for efflux of bicarbonate. Clearance studies reveal that carbonic anhydrase dependent and independent bicarbonate reabsorption are not saturable but depend on the rate of volume reabsorption in the kidney. In conclusion, passive movements of bicarbonate do occur in proximal convoluted tubules and most likely contribute to carbonic anhydrase independent bicarbonate reabsorption.

Absorption↗
PubMed1982

Cellular Mechanism of the furosemide sensitive transport system in the kidney.

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. The experiments further suggest that potassium ions are involved in the sodium chloride transport system because potassium reabsorption is inhibited by furosemide and because intracellular sodium falls significantly when potassium ions are removed from the tubular fluid. Furthermore, there is experimental evidence that the luminal potassium uptake mechanism is suppressed after potassium adaptation. Under these conditions potassium transport is found to be insensitive to furosemide. The data suggest a furosemide sensitive cotransport system for sodium, chloride and potassium, operative in the luminal cell membrane. The energy for this carrier-mediated transport process is provided by the large "downhill" gradient of sodium across the luminal cell membrane which is maintained by the sodium pump located in the peritubular cell membrane.

Animals↗
PubMed1982

Effects of inhibition of chloride transport on intracellular sodium activity in distal amphibian nephron.

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. The present experiments were carried out to evaluate directly the electrochemical driving forces acting on sodium ions under similar experimental conditions. Intracellular sodium activity measurements were performed in the doubly-perfused kidney of Amphiuma by means of single-barreled liquid ion-exchange microelectrodes. Basolateral cell membrane potential and resistance ratio measurements of tubular cell membranes were also carried out under control conditions and after inhibition of chloride transport by luminal application of furosemide (5 . 10(-5) mol/l) or by omission of chloride. Control conditions were characterized by a steep downhill electrochemical gradient for sodium ions from lumen to cell. Inhibition of chloride transport led to a sharp decrease of intracellular sodium activity and to hyperpolarization of the peritubular membrane potential while the resistance ratio of the tubular cell membranes did not change significantly. These results demonstrate the presence of low cellular sodium activities in early distal tubule cells. The sharp decline of cell sodium after furosemide and after luminal chloride removal is consistent with inhibition of a sodium chloride cotransport system and continued peritubular sodium extrusion. The latter can increase the electrochemical gradient of sodium ions beyond that observed under control conditions.

Animals↗
PubMed1982

The effect of respiratory and metabolic acid-base changes on ionized calcium concentration: in vivo and in vitro experiments in man and rat.

Correlation of ionized calcium concentration, [Ca2+] and blood pH has long been recognized. So far no distinction of the acid-base changes, i.e. respiratory changes or metabolic changes seemed necessary. The present study, with the use of a recently developed system for in vivo analysis of [Ca2+], and with in vitro experiments reinvestigates this question. In a first series respiratory and metabolic changes were induced in rats. Changes of [Ca2+] (delta [Ca2+]) and of plasma pH (delta pH) were recorded continuously in vivo, plasma bicarbonate, [HCO-3] was measured in vitro. In a second series respiratory and metabolic changes were induced in sixteen volunteers and, separately, in vitro in plasma and modified Ringer solution, and the same parameters were determined. In all experiments delta [Ca2+] correlates negatively with delta pH. However, the correlation in respiratory changes was significantly less as compared to that in metabolic changes. As expected, delta [HCO-3] correlates positively with pH in metabolic and negatively in respiratory changes. We conclude from these experiments that in metabolic changes the effects of calcium-albumin interaction and calcium complexation with bicarbonate are additive, whereas both effects oppose each other in respiratory changes. This might explain the blunted effect of pH changes on [Ca2+] in respiratory changes.

Acidosis↗