Biomedical subjects

G Stange

Publications and source records attributed to G Stange.

At least 55 records · Page 3Linked to original sources

PubMed1987

Identification of proximal tubular transport functions in the established kidney cell line, OK.

OK cells, derived from an American opossum kidney, were analyzed for proximal tubular transport functions. In monolayers, L-glutamate, L-proline, L-alanine, and alpha-methyl-glucopyranoside (alpha-methyl D-glucoside) were accumulated through Na+-dependent and Na+-independent transport pathways. D-Glucose and inorganic sulfate were accumulated equally well in the presence or absence of Na+. Influx of inorganic phosphate was only observed in the presence of Na+. Na+/alpha-methyl D-glucoside uptake was preferentially inhibited by phlorizin and D-glucose uptake by cytochalasin B. An amiloride-sensitive Na+-transport was also identified. In isolated apical vesicles (enriched 8-fold in gamma-glutamyltransferase), L-glutamate, L-proline, L-alanine, alpha-methyl D-glucoside and inorganic phosphate transport were stimulated by an inwardly directed Na+-gradient as compared to an inwardly directed K+-gradient. L-Glutamate transport required additionally intravesicular K+. D-Glucose transport was similar in the presence of a Na+- and a K+-gradient. Na+/alpha-methyl D-glucoside uptake was inhibited by phlorizin whereas cytochalasin B had no effect on Na+/D-glucose transport. An amiloride-sensitive Na+/H+ exchange mechanism was also found in the apical vesicle preparation. It is concluded that the apical membrane of OK cells contains Na+-coupled transport systems for amino acids, hexoses, protons and inorganic phosphate. D-Glucose appears a poor substrate for the Na+/hexose transport system.

Amino Acids↗

PubMed1987

Calcium uptake into rat small intestinal brush border membrane vesicles: characterization of transmembrane calcium transport at short initial incubation times.

Calcium transport into brush border vesicles from rat small intestine was investigated by determining uptake rates at very short incubation periods. At incubation times up to 1 second a linear relationship between calcium uptake and time was observed at free calcium concentrations ranging from 1 microM to 5 mM. At time points above 1 second calcium uptake deviates progressively from linearity. Several lines of evidences (EGTA-wash, dependency on membrane potential, temperature sensitivity and effect of the calcium ionophore A23187) suggest transmembrane transport rather than extravesicular binding of calcium as being responsible for calcium uptake. Saturation experiments performed under initial linear and curvilinear uptake conditions show a saturable transport component in the mu molar and only a tendency to saturate in the molar concentration range. It is concluded that uptake values far from equilibrium are characteristic for transmembrane flux of calcium. Transmembrane flux of calcium is mediated by multiple and potential-sensitive mechanisms.

Animals↗

PubMed1986

Sodium-proton exchange in colon brush-border membranes.

Apical membrane vesicles were prepared from proximal and distal segments of the large intestine of the rat by a method based on morphological criteria and were used to determine 22Na uptake. In both preparations an outwardly directed proton gradient stimulated 22Na uptake. In proximal colon a decrease in vesicular volume induced by an increased media osmolarity led to diminished 22Na uptake at 90 min; a significant (50-60%) portion of uptake represented binding. Initial uptake was linear for 10 s and extrapolated through zero, indicating minimal extravesicular binding. Initial uptake was a saturable function of medium Na concentration. In both preparations initial influx of 0.1 mM NaCl was inhibited by amiloride (0.1-1.0 mM), 15 mM NaCl, 15 mM LiCl, and 15 mM NH4Cl. From the characteristics of the initial 22Na influx we conclude that the apical membrane from colonocytes of proximal and distal segments contains a Na-H exchange with properties similar to those described in other epithelia.

Amiloride↗

PubMed1986

[Functional characterization of luminal enterocyte membranes of the small intestine mucosa using isolated brush border membranes].

Atrophy of the small intestinal mucosa is functionally characterized by a reduction in non-electrolyte transport in vivo. In order to elucidate the cellular defect being responsible for this malabsorption, we have studied the Na+-dependent D-glucose accumulation as well as the activities of aminopeptidase M and maltase in brush border membrane vesicles prepared from jejunal self-emptying blind loops and corresponding intestinal segments of sham-operated control rats. Membrane vesicles from atrophic mucosa did not show any differences in D-glucose uptake or in enzyme activities when compared with those derived from normal intestine. Thus it is unlikely that the impaired non-electrolyte absorption in the atrophic mucosa in vivo is due to a defect in cellular transport processes. It is more probable that the functional impairment is the result of the diminished absorptive surface in this pathophysiological condition.

Aminopeptidases↗

PubMed1985

Defective jejunal brush-border Na+/H+ exchange: a cause of congenital secretory diarrhoea.

In a child with congenital secretory diarrhoea, jejunal perfusion studies showed net water and electrolyte secretion and suggested a defect in sodium/proton exchange. A technique was developed for investigation of such exchange in brush-border membrane vesicles from jejunal biopsy specimens. Vesicles from control specimens displayed proton-gradient-dependent sodium uptake, whereas those from the patient did not. These findings, as well as pointing to a cause of congenital secretory diarrhoea, confirm the existence and importance of jejunal sodium/proton exchange in man.

Cell Membrane↗

PubMed1985

Transport of sulphate in rat jejunal and rat proximal tubular basolateral membrane vesicles.

Basolateral membrane vesicles were isolated by a Percoll density gradient centrifugation method from small intestinal and renal proximal tubular epithelial cells. Transport of sulphate across the basolateral membrane was analyzed by measuring the uptake of tracer sulphate. In both membrane preparations, preloading the vesicles with sulphate- or hydroxyl-anions stimulated tracer sulphate uptake (trans-stimulation); an inwardly directed sodium gradient did not stimulate sulphate influx whether in the absence or in the presence of sulphate- or hydroxyl-ion-trans-stimulation. Under sulphate trans-stimulation conditions, DIDS (10(-4) mol/l) inhibited sulphate influx. In intestinal membranes, trans-stimulation of sulphate influx was obtained by preloading the vesicles with chloride, in renal membranes by preloading with bicarbonate. Under sulphate trans-stimulation conditions, in intestinal membranes, sulphate influx was strongly inhibited by chloride, in renal membranes, chloride inhibition was absent. Under bicarbonate trans-stimulation conditions, in renal membranes, sulphate transport was inhibited by lactate. It is concluded that small intestinal and renal proximal tubular basolateral membrane vesicles contain a transport mechanism for sulphate that cannot be energized by a sodium gradient. The transport system in small intestinal basolateral membranes seems to be different from that in renal membranes. It is suggested that the observed interaction between inorganic and organic anion transport in renal basolateral membranes is indirect.

Animals↗

PubMed1984

Intravesicular NAD has no effect on sodium-dependent phosphate transport in isolated renal brush border membrane vesicles.

The effects of intravesicular NAD on Na+-dependent 32Pi uptake were investigated in isolated rat kidney brush border membrane vesicles (BBMV). NAD was introduced into the vesicles by osmotic shock, and extravesicular NAD was removed by passing the vesicles through a anion exchange column. The effectiveness of the osmotic shock procedure and the hydrolysis of extra- and intravesicular NAD were controlled by enzymatic analysis and thin layer chromatography. ADP-ribosylation of the membrane proteins was analyzed in vesicles osmotically shocked in the presence of either [adenylate-32P]-NAD or [adenine-2,8-3H]-NAD by SDS-polyacrylamide gel electrophoresis. It was found that the Na+-dependent Pi uptake was inhibited when the BBMV were incubated with NAD at alkaline pH, which resulted in rapid NAD hydrolysis. When NAD was present in the intravesicular space only, the Na+-dependent Pi uptake was not inhibited. 32P from NAD was rapidly incorporated into a number of brush border membrane proteins, but no incorporation of 3H-adenine could be detected. The results provide evidence that NAD does not inhibit Pi transport by a direct interaction with the cytoplasmic side of the brush border membrane. No evidence of ADP-ribosylation of the brush border membrane protein(s) was found.

Animals↗

PubMed1983

Transport of L-lysine by rat renal brush border membrane vesicles.

L-3H-lysine uptake into brush border membrane vesicles was measured by a rapid filtration technique. A significant binding of L-lysine at the vesicle interior was observed. Extrapolating initial linear uptake to zero incubation time did not indicate binding of the amino acid to the external membrane surface. Sodium stimulated the L-lysine uptake specifically. Experiments in the presence of potassium/valinomycin induced diffusion potentials, and experiments with a potential sensitive fluorescent dye documented an electrogenic uptake mechanism for L-lysine only in the presence of sodium. Sodium independent uptake proceeds via an electroneutral pathway. Transstimulation experiments show carrier mediated uptake in the presence and absence of sodium. An outwardly directed proton-gradient stimulated L-lysine uptake in the presence and absence of sodium. Saturation of L-lysine uptake was observed in the presence and absence of sodium. In the absence of sodium, L-lysine uptake was inhibited by L-arginine, L-cystine, L-phenylalanine and L-methionine. The sodium dependent uptake was inhibited by L-arginine and L-cysteine; small inhibition by L-phenylalanine was observed. In the presence or absence of sodium, L-lysine uptake was inhibited neither by D-lysine nor by L-glutamic acid. These results document carrier mediated transport of L-lysine via (a) transport mechanism(s) not obligatory requiring sodium.

Amino Acids↗

PubMed1983

Transport of L-cystine by rat renal brush border membrane vesicles.

Brush border membranes were isolated from rat renal cortex by a divalent cation precipitation method. L-35S-cystine uptake into the vesicles was measured by a rapid filtration method. Covalent incorporation of tracer into membrane proteins was observed after prolonged incubations. At short incubation periods (1 min) binding was small and allowed an analysis of transmembrane transport. To guarantee transport of L-cystine, the experiments were performed in the presence of the oxidant diamide. Sodium stimulated L-cystine uptake specifically. A potassium/valinomycin induced inside negative diffusion potential stimulated sodium dependent L-cystine transport. Thus, transport is potential sensitive in the presence of sodium. At low substrate and inhibitor concentrations, L-cystine transport was inhibited by L-lysine, L-ornithine and L-arginine but not by D-lysine in the presence and absence of sodium. At higher inhibitor concentration, the neutral amino acids L-phenylalanine and L-leucine also inhibited L-cystine uptake, but only the sodium dependent uptake. These inhibition experiments suggest that L-cystine is transported by the brush border membrane by a transport system for basic amino acids not necessarily requiring sodium. In addition, transport of L-cystine can also proceed via sodium dependent transport pathways for neutral amino acids. In the concentration range tested (up to 0.225 mmoles/l), no saturation of L-cystine transport was observed in the presence and absence of sodium.

Amino Acids↗

PubMed1983

Transport of L-cysteine by rat renal brush border membrane vesicles.

Brush border membranes were isolated from rat renal cortex by a divalent cation precipitation method. L-35S-cysteine uptake into the vesicles was measured by a rapid filtration method. Only minimal binding of the amino acid to the vesicles was observed. Sodium stimulates L-cysteine uptake specifically. Anion replacement experiments, experiments in the presence of potassium/valinomycin-induced diffusion potential as well as experiments with a potential-sensitive fluorescent dye document an electrogenic sodium-dependent uptake mechanism for L-cysteine. Tracer replacement experiments as well as the fluorescence experiments indicate a preferential transport of L-cysteine. Transport of L-cysteine is inhibited by L-alanine and L-phenylalanine but not by L-glutamic acid and the L-basic amino acids. Initial, linear influx kinetics provide evidence for the existence of two transport sites. The results suggest (a) sodium-dependent mechanism(s) for L-cysteine shared by other neutral amino acids.

Alanine↗

PubMed1982

[Variation of the tinnitus on moist tubotympanical catarrh and otosclerosis before and after operation (author's transl)].

The tinnitus on moist tubotympanical catarrh and otosclerosis had been registered before and after the operation in relation to the frequence and the audibility. 222 children ears and 55 adult with a moist tubotympanical catarrh had been studied. Of these 28 children 26 adult ears had a tinnitus. After the operation and after using a "Donaldson silicone Drain Tube" without relation of the tinnitus there had been reached a very good win of hearing and excepted for 6 adults, whose tinnitus only had been lower, and elimination of the tinnitus. In 65 patients from 71 patients with stapedectomy it was able to look out for the tinnitus before and after the operation. Before the operation 44 patients had no tinnitus and 21 patients had a very disagreeable tinnitus; 17 patients from these had after the stapedectomy no longer a tinnitus. The audibility of the tinnitus from 4 patients had been reduced very much. The result of hearing the management of the inner ear after the operation haven't had any relation to the tinnitus before the operation.

Adolescent↗

PubMed1981

Sulfate-sodium cotransport by brush-border membrane vesicles isolated from rat ileum.

Uptake of inorganic sulfate into brush-border membrane vesicles isolated by a calcium precipitation method from rat small intestine was investigated using a rapid filtration technique and 35Sulfur acid as tracer. Sulfate uptake by membrane vesicles was osmotically sensitive, suggesting transport into an intravesicular space rather than binding to or incorporation into the membrane. Transport of sulfate into brush-border vesicles isolated from rat ileum was only stimulated by sodium ions as compared with other monovalent cations. A typical "overshoot" phenomenon was observed in the presence of an inwardly directed NaCl gradient. Tracer sulfate exchange was faster in the presence of sodium than in the presence of potassium. Addition of the ionophores for monovalent cations, monactin, or gramicidin D, decreased the sodium gradient-driven sulfate uptake. Sulfate uptake showed a saturation phenomenon only in the presence of sodium. Transstimulaton of sodium-dependent sulfate transport was shown with MoO4(2-), but not with PO4(2-) and WO4(2-). Changing the electrical potential difference across the membrane vesicles by establishing different diffusion potentials (anion replacement; potassium gradient +/- valinomycin) did not alter sodium-dependent sulfate uptake. Stimulation of sulfate transport by sodium was greater in membrane vesicles from ileal segments than from duodenum or jejunum. It is concluded that isolated brush-border membranes of rat ileum contain an electroneutrol sodium-sulfate cotransport system.

Animals↗

PubMed1980

The effects of potassium and membrane potential on sodium-dependent glutamic acid uptake.

The uptake of L-glutamic acid into brush-border membrane vesicles isolated from rat renal proximal tubules is NA+-dependent. In contrast to Na+-dependent uptake of D-glucose, pre-equilibration of the vesicles with K+ stimulates L-glutamic acid uptake. Imposition of a K+ gradient ([Ki+] > [Ko+]) further enhances Na+-dependent L-glutamic acid uptake, but leaves K+-dependent glucose transport unchanged. If K+ is present only at the outside of the vesicles, transport is inhibited. Intravesicular Rb+ and, to a lesser extent, Cs+ can replace intravesicular K+ to stimulate L-glutamic acid uptake. Changes in membrane potential incurred by the imposition of an H+-diffusion potential or anion replacement markedly affect Na+-dependent glutamic acid uptake only in the presence of K+. Experiments with a potential-sensitive cyanine dye also indicate that, in the presence of intravesicular K+ a charge movement is involved in Na+-dependent transport of L-glutamic acid. The data indicate that Na+-dependent L-glutamic acid transport can be additionally energized by a K+ gradient. Furthermore, intravesicular K+ render Na+-dependent L-glutamic acid transport sensitive to changes in the transmembrane electrical potential difference.

Animals↗

PubMed1980

[The use of ultra-sound in sinus disease (author's transl)].

The inclusion of ultra-sound in the routine diagnosis of sinus disease reduces the margin of error by about 6%, compared to that using clinical records and x-ray. The investigator should have sufficient experience in operating the ultrasonic equipment. Especially valuable is the ultrasonic diagnosis in cases of discharge, mucosal swelling or tumor in the sinus, as well as in cases of sinus examination of children and for control of patients having had conservative treatment or operations.

Child, Preschool↗

PubMed1979

Sulphate-ion/sodium-ion co-transport by brush-border membrane vesicles isolated from rat kidney cortex.

Uptake of SO(4) (2-) into brush-border membrane vesicles isolated from rat kindey cortex by a Ca(2+)-precipitation method was investigated by using a rapid-filtration technique. Uptake of SO(4) (2-) by the vesicles was osmotically sensitive and represented transport into an intra-vesicular space. Transport of SO(4) (2-) by brush-border membranes was stimulated in the presence of Na(+), compared with the presence of K(+) or other univalent cations. A typical ;overshoot' phenomenon was observed in the presence of an NaCl gradient (100mm-Na(+) outside/zero mm-Na(+) inside). Radioactive-SO(4) (2-) exchange was faster in the presence of Na(+) than in the presence of K(+). Addition of gramicidin-D, an ionophore for univalent cations, decreased the Na(+)-gradient-driven SO(4) (2-) uptake. SO(4) (2-) uptake was only saturable in the presence of Na(+). Counter-transport of Na(+)-dependent SO(4) (2-) transport was shown with MoO(4) (2-) and S(2)O(3) (2-), but not with PO(4) (2-). Changing the electrical potential difference across the vesicle membrane by establishing different diffusion potentials (anion replacement; K(+) gradient+/-valinomycin) was not able to alter Na(+)-dependent SO(4) (2-) uptake. The experiments indicate the presence of an electroneutral Na(+)/SO(4) (2-)-co-transport system in brush-border membrane vesicles isolated from rat kidney cortex.

Animals↗

PubMed1979

[Ultrasonic diagnosis and sinus diseases].

By employing ultrasound in the routine diagnosis of sinus diseases, the margin of error in the accuracy of diagnosis can be reduced by 10% compared to that using clinical records and x-rays, provided however, that the investigator has sufficient experience in operating the ultrasonic equipment. The inclusion of ultrasonic diagnostics has proven itself particularly valuable in the diagnosis if both discharges and tumors in children and for progress control of patients having had conservative treatment or operations.

Humans↗

PubMed1979

The effect of harmaline on intestinal sodium transport and on sodium-dependent D-glucose transport in brush-border membrane vesicles from rabbit jejunum.

Harmaline inhibition of sodium uptake and of sodium-dependent D-glucose transport was investigated using brush-border membrane vesicles from frozen rabbit jejunum. Under sodium-gradient conditions, "initial" D-glucose uptake (20 s) was inhibited by harmaline at concentrations above 0.5 mM, but at lower harmaline concentrations D-glucose uptake was stimulated by 10--15%. When a similar potassium gradient was used, harmaline had no effect. At concentrations up to 2 mM, harmaline did not alter the equilibrium uptake of D-glucose or D-mannitol. After pre-equilibration with sodium (25 mM), G-glucose uptake was inhibited at harmaline concentrations ranging from 0.1 to 2 mM. Sodium (10 mM) uptake was also inhibited by harmaline. Increasing the sodium concentration reduced the inhibitory effect of harmaline on tracer sodium uptake as well as on sodium-dependent D-glucose uptake. Similar to phlorizin, harmaline (1 mM) was able to prevent glucose-induced sodium influx across the brush-border membrane. Sodium uptake into brush-border membrane vesicles seems to be inhibited at lower harmaline concentrations than sodium-dependent D-glucose uptake. At high (2 mM) inhibitor concentrations, however, sodium-dependent glucose uptake is more strongly inhibited than sodium uptake. These results suggest that harmaline inhibits both sodium and sodium-dependent transport across intestinal brush-border membranes by interacting with specific sodium-binding sites.

Alkaloids↗

PubMed1978

Taurocholate--sodium co-transport by brush-border membrane vesicles isolated from rat ileum.

Uptake of taurocholate into brush-border membrane vesicles isolated from rat small intestine by a Ca(2+) -precipitation method was investigated by using a rapid-filtration technique. Uptake of taurocholate by ileal brush-border membranes consisted of three phenomena: binding to the outside of the vesicles, transfer across the vesicle membrane and binding to the intravesicular compartment. The transport of taurocholate across the brush-border membranes was stimulated in the presence of Na(+) compared with the presence of K(+); stimulation was about 11-fold in the presence of a NaCl gradient (Na(o)>Na(i)), where the subscripts refer to ;outside' and ;inside' respectively, and 4-fold under equilibrium conditions for Na(+) (Na(o)=Na(i)). In the presence of a Na(+) gradient a typical ;overshoot' phenomenon was observed. Membranes preloaded with unlabelled taurocholate showed an accelerated entry of labelled taurocholate (tracer exchange) in the presence of Na(+) compared with the presence of K(+). The stimulation by Na(+) was observed only in membrane preparations from the ileum. Addition of monactin, an ionophore for univalent cations, decreased the Na(+)-gradient-driven taurocholate uptake. The Na(+)-dependent taurocholate transport showed saturation kinetics and the phenomenon of counterflow and was inhibited by glycocholate. Other cations such as Li(+), Rb(+) and Cs(+) could not replace Na(+) in its stimulatory action. When the electrical potential difference across the vesicle membrane was altered by establishing different diffusion potentials (anion replacement; K(+) gradient+/-valinomycin) a more-negative potential inside stimulated Na(+)-dependent taurocholate transport. These data demonstrate the presence of a rheogenic (potential sensitive) Na(+)-taurocholate co-transport system in ileal brush-border membranes and support the hypothesis that the reabsorption of bile acids in the ileum is a secondary active uptake.

Animals↗