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H Oberleithner

Publications and source records attributed to H Oberleithner.

At least 127 records · Page 7Linked to original sources
PubMed1985

Intracellular pH in diluting segment of frog kidney.

Chronic exposure to high potassium (K+ adaptation) stimulates H+ net secretion in the diluting segment of the frog kidney. In order to investigate the cellular mechanism of the H+ secretory process intracellular pH (pHi) measurements were performed in cells of the diluting segment of the isolated doubly-perfused kidney of K+ adapted Rana esculenta. pHi changes were monitored by pH-sensitive microelectrodes while the tubule lumen was rapidly perfused with various solutions. With control solutions (extracellular pH = 7.80) pHi averaged 7.60 +/- 0.05. Luminal application of furosemide (5 X 10(-5) mol/l) or reduction of luminal Cl- (from 104 mmol/l to 9 mmol/l) hyperpolarized the cell membrane potentials but pHi was not altered. Reduction of luminal Na+ (from 98 mmol/l to 3 mmol/l) depolarized the cell membrane potentials but pHi remained constant. Complete removal of luminal Na+, however, led to a significant decrease of pHi from 7.61 +/- 0.08 to 7.18 +/- 0.08. Luminal application of amiloride (1 X 10(-3) mol/l) also decreased pHi significantly (delta pHi = 0.15 +/- 0.02). The results indicate that an amiloride-sensitive H+ extrusion mechanism exists in the luminal cell membrane of the K+ adapted frog diluting segment. The data are consistent with Na+/H+ exchange which maintains a constant pHi even at extreme experimental conditions.

Amiloride↗
PubMed1985

Relationship between luminal Na+/H+ exchange and luminal K+ conductance in diluting segment of frog kidney.

Experiments were performed in the isolated perfused kidney of K+ adapted Rana pipiens to investigate the relationship between luminal K+ conductance and H+ transport in cells of the diluting segment. Inhibition of luminal Na+/H+ exchange by amiloride or by omission of luminal Na+ blocked luminal K+ conductance. Acidification of the kidney perfusate by elevation of pCO2 also reduced luminal K+ conductance. This effect could be prevented by furosemide. Since the steepest transcellular Na+ potential difference, directed from the lumen into the cell, is found when luminal Na+/Cl-/K+ cotransport is inhibited by furosemide, we conclude that luminal Na+/H+ exchange is most efficient at these conditions and thus could attenuate intracellular acidification.

Amiloride↗
PubMed1985

Ouabain decreases apparent potassium-conductance in proximal tubules of the amphibian kidney.

According to a previous study from this laboratory, the electrochemical gradient for potassium across the peritubular cell membrane of proximal tubules in the isolated perfused frog kidney increases following the application of ouabain. In order to test, if this phenomenon were due to a decrease of potassium conductance, the effects of ouabain on cell membrane resistances and the sensitivity of the peritubular cell membrane potential difference (PDpt) to step changes of peritubular potassium and bicarbonate concentration were studied. In the absence of ouabain, PDpt averaged -60 +/- 3 mV (n = 25). A step increase of peritubular potassium concentration from 3 to 18 mmol/l (pH 8.07) depolarizes PDpt (delta PDk) by +24 +/- mV (n = 8). An increase of bicarbonate from 20 to 40 mmol/l (pH 8.07) hyperpolarizes PDpt (delta PDb) by -2.8 +/- 0.4 mV (n = 9). The resistance of the luminal and peritubular cell membranes in parallel (Rm) amounts to 45 +/- 9 k omega cm (tubule length) (n = 4) and the voltage divider ratio (VDR) to 1.4 +/- 0.2 (n = 7). The resistance of the cellular cable (cellular core, Rc) approaches 131 +/- 37 M omega/cm (n = 4). Peritubular application of 0.1 mmol/l ouabain leads to a gradual decline of PDpt (t1/2 approx. 30 min), to an increase of Rm, a decrease of delta PDk and an increase of delta PDb. VDR and Rc are not changed significantly. The data point to a functional link between the sodium/potassium ATPase and the potassium conductance of the peritubular cell membrane.

Animals↗
PubMed1985

The effect of phenylalanine on the electrical properties of proximal tubule cells in the frog kidney.

The present study was designed to elucidate the effects of sodium-coupled transport on the electrical properties of proximal tubule cells in the isolated perfused frog kidney. Cable analysis techniques have been employed to determine the resistance of the luminal and peritubular cell membranes in parallel (Rm) and the apparent ratio of the luminal over the peritubular cell membrane resistance (VDR). Furthermore, the sensitivity of the potential difference across the peritubular cell membrane (PDpt) to 6-fold increases of peritubular potassium concentration (delta PDk) was taken as a measure of the relative potassium conductance of this membrane. In the absence of luminal phenylalanine, PDpt amounts to -60 +/- 1 mV (n = 90), Rm to 36 +/- 3 k omega cm (n = 22), VDR to 1.81 +/- 0.14 (n = 20), and delta PDk to 15.0 +/- 0.9 mV (n = 25). The application of 10 mmol/l phenylalanine replacing 10 mmol/l raffinose leads to a rapid (within 30 s) depolarisation of PDpt to 50 +/- 5% of its control value and to a delayed (within 12 min) recovery to 95 +/- 5% of control. The rapid depolarisation is associated with a decline of Rm and VDR, indicating a decrease mainly of the luminal cell membrane resistance. During recovery of PDpt there is a parallel increase of VDR and a further decline of Rm pointing to a decline of the basolateral cell membrane resistance. Delta PDk is decreased during rapid depolarisation but increases again during the recovery phase. Thus, phenylalanine initially decreases but then increases above control the apparent potassium conductance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Resistance properties of the diluting segment of Amphiuma kidney: influence of potassium adaptation.

Chronic exposure to high potassium stimulates K+-secretory mechanisms in the diluting segment of the amphibian kidney (K+ adaptation). Since K+ net flux depends critically on the passive cell membrane permeabilities for K+ ions, cable analysis and K+-concentration step changes were applied in this nephron segment to assess the individual resistances of the epithelium and the K+ conductance of the luminal cell membrane. Experiments were performed in the isolated, doubly-perfused kidney of both control and K+-adapted Amphiuma. In control animals transepithelial resistance was 290 +/- 27 omega cm2, which decreased significantly to 199 +/- 17 omega cm2 after K+ adaptation. The resistance in parallel of the luminal and peritubular cell membrane decreased from a control value of 157 +/- 14 to 108 +/- 6 omega cm2 after chronic K+ treatment. This was paralleled by a decrease of the ratio of the luminal to peritubular cell membrane resistance from 2.5 +/- 0.1 to 1.9 +/- 0.1, respectively. Estimation of the individual cell membrane resistances reveals that the combined resistance of the luminal and peritubular cell membrane is in the same order of magnitude as the paracellular shunt resistance in diluting segments of both control and K+-adapted animals. The luminal cell membrane is K+ selective under both conditions, but the absolute luminal K+ conductance increases by some 60% with K+ adaptation. This leads to an increased back-leak of K+ from cell to lumen and may explain stimulated K+ net secretion found after chronic K+ loading.

Adaptation, Physiological↗
PubMed1985

Relationship between cell volume and ion transport in the early distal tubule of the Amphiuma kidney.

The roles of apical and basolateral transport mechanisms in the regulation of cell volume and the hydraulic water permeabilities (Lp) of the individual cell membranes of the Amphiuma early distal tubule (diluting segment) were evaluated using video and optical techniques as well as conventional and Cl-sensitive microelectrodes. The Lp of the apical cell membrane calculated per square centimeter of tubule is less than 3% that of the basolateral cell membrane. Calculated per square centimeter of membrane, the Lp of the apical cell membrane is less than 40% that of the basolateral cell membrane. Thus, two factors are responsible for the asymmetry in the Lp of the early distal tubule: an intrinsic difference in the Lp per square centimeter of membrane area, and a difference in the surface areas of the apical and basolateral cell membranes. Early distal tubule cells do not regulate volume after a reduction in bath osmolality. This cell swelling occurs without a change in the intracellular Cl content or the basolateral cell membrane potential. In contrast, reducing the osmolality of the basolateral solution in the presence of luminal furosemide diminishes the magnitude of the increase in cell volume to a value below that predicted from the change in osmolality. This osmotic swelling is associated with a reduction in the intracellular Cl content. Hence, early distal tubule cells can lose solute in response to osmotic swelling, but only after the apical Na/K/Cl transporter is blocked. Inhibition of basolateral Na/K ATPase with ouabain results in severe cell swelling. This swelling in response to ouabain can be inhibited by the prior application of furosemide, which suggests that the swelling is due to the continued entry of solutes, primarily through the apical cotransport pathway.

Animals↗
PubMed1984

The effect of ouabain on intracellular activities of K+, Na+, Cl-, H+ and Ca2+ in proximal tubules of frog kidneys.

Using conventional and ion selective microelectrodes, the effect of ouabain (10(-4) mol/l) on peritubular cell membrane potential (PDpt), on intracellular pH (pHi) as well as on the intracellular ion activities of Cl- (Cli-), K+ (Ki+), Na+ (Nai+) and Ca2+ (Ca2i+) was studied in proximal tubules of the isolated perfused frog kidney. In the absence of ouabain (PDpt = -57.0 +/- 1.9 mV), the electrochemical potential difference of chloride (apparent mu Cl- = -22 +/- 2 mV) and of potassium (mu K+ = +24 +/- 3 mV) is directed from cell to bath, of H+ (mu H+ = -42 +/- 5 mV), of Na+ (mu Na+ = -102 +/- 4 mV) and of Ca2+ (mu Ca2+ = -148 +/- 6 mV) from bath to cell. Ouabain leads to a gradual decline of PDpt, which is reduced to half (PDpt, 1/2) within 31 +/- 4.6 min (in presence of luminal glucose and phenylalanine), and to a decline of the absolute values of apparent mu Cl+, of mu H+, mu Na+ and mu Ca2+. In contrast, an increase of mu K+ is observed. At PDpt, 1/2 apparent Cl-i increases by 6.2 +/- 1.0 mmol/l, pHi by 0.13 +/- 0.03, Ca2+i by 185 +/- 21 nmol/l, and Nai+ by 34.2 +/- 4.6 mmol/l, whereas Ki+ decreases by 37.7 +/- 2.2 mmol/l. The results suggest that the application of ouabain is followed by a decrease of peritubular cell membrane permeability to K+, by an accumulation of Ca2+, Na+ and HCO3- in the cell and by a dissipation of the electrochemical Cl- gradient.

Animals↗
PubMed1984

The influence of intracellular sodium activity on the transport of glucose in proximal tubule of frog kidney.

Inhibition of basolateral Na+/K+ ATPase by ouabain eventually abolishes transport of glucose. The present study was performed to test, if this effect is due to a dissipation of the electrochemical gradient for sodium or due to a regulatory inhibition of sodium-coupled glucose entry across the luminal membrane at increasing intracellular sodium activity. To this end, proximal convoluted tubules of the doubly perfused isolated frog kidney were perfused alternatively with solutions containing either 5 mmol/l glucose or raffinose. The potential difference across the peritubular cell membrane (PDpt) and across the epithelium (PDte) has been recorded with conventional and across the peritubular cell membrane with ion selective microelectrodes (PDpt). In the absence of luminal glucose PDpt is (+/- SEM) -54.0 +/- 2.4 mV, PDte = -1.2 +/- 2.0 mV and PDNapt = -96 +/- 5 mV. The electrochemical gradient for sodium (mu Na+) amounts to 95 mV and intracellular sodium activity to 14 mmol/l (extracellular sodium activity is 74 mmol/l). Luminal application of glucose leads to a rapid depolarisation of PDpt (delta PDpt = 8.6 +/- 0.9 mV and PDNapt (delta PDNapt = 11.1 +/- 3.0 mV) and to hyperpolarisation of PDte (delta PDte = -0.8 +/- 0.2 mV). The peritubular application of ouabain leads to a gradual, reversible and proportional decline of PDpt, PDNapt and mu Na+. Glucose induced delta PDpt and delta PDNapt decrease in parallel to PDpt and PDNapt, resp. In a separate series, the lumped conductance (Gm) of the luminal and basolateral cell membrane has been determined, which amounts to 2.4 +/- 0.3 microS/mm (tubule length). Gm decreases 23 +/- 4%, when PDpt is decreased to half.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Cytotoxic effect of choline, abolished by furosemide, in the diluting segment of frog kidney.

Previous observations suggest that luminal application of tetra-N-alkylammonium ions may impair ion transport in the amphibian diluting segment. To investigate this question conventional KCl-filled and Cl- sensitive microelectrodes were applied in diluting segments of the isolated perfused kidney of rana esculenta to evaluate transepithelial electrical and chloride electrochemical (PDte, EClte) as well as peritubular cell membrane potential difference (PDpt), measured at static head conditions. After determination of control values the tubule lumen was exposed to choline (95 mmol/l, substituted for Na+) both in presence or absence of furosemide (5 X 10(-5) mol/l). Then, the lumen was again perfused with control solution and the measurements were repeated. Thus, a time course for possible choline induced effects was obtained both in the presence and absence of furosemide. The lumen positive PDte decreased from 11.2 +/- 1.0 mV to 6.3 +/- 0.8 mV after 2 min and to 1.9 +/- 0.4 mV after 30 min exposure to choline. PDpt (cell interior negative) decreased from 70 +/- 2 mV to 58 +/- 3 mV and to 42 +/- 5 mV after 2 and 30 min, respectively. Intraluminal Cl- activity increased from its initial steady state value of 20 +/- 2 mmol/l to 39 +/- 2 mmol/l after 30 min exposure to choline. However, if the tubule lumen was exposed to choline in presence of furosemide (5 X 10(-5) mol/l), all the above described choline-induced effects did not become apparent.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Mechanism of hydrogen ion transport in the diluting segment of frog kidney.

Transepithelial H+ transport was studied in diluting segments of the isolated-perfused kidney of rana esculenta. The experiments were performed in controls as well as in K+-adapted and Na+-adapted animals (exposed to 50 mmol/l KCl or NaCl, resp. for at least 3 days). Conventional and single-barreled, liquid ion-exchanger H+-sensitive microelectrodes were applied in the tubule lumen to evaluate transepithelial H+ net flux (JHte) as well as limiting transepithelial electrical and H+ electrochemical potential differences (PDte, EHte) and luminal pH at zero net flux conditions. The measurements were made in absence (control) and presence of furosemide (5 X 10(-5) mol/l) or amiloride (10(-3) mol/l). EHte (lumen positive vs ground) was 19 +/- 3 mV in controls, 43 +/- 3 mV in K+ adapted but about zero in Na+ adapted animals. Using the corresponding PDte-values, steady state luminal pH of 7.63 +/- 0.05, 7.13 +/- 0.05 and 8.02 +/- 0.02 was calculated for the respective groups of animals (peritubular pH 7.80). In parallel, significant secretory JHte (from blood to lumen) was found in controls (14 +/- 2 pmol X cm-2 X s-1) which was stimulated by K+ adaptation (61 +/- 8 pmol X cm-2 X s-1) but reversed in direction by Na+-adaptation (-8 +/- 1 pmol X cm-2 X s-1). Amiloride inhibited secretory JHte.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1984

A microelectrode for continuous monitoring of glucose concentration in isolated perfused tubule segments.

The design and the application of a micro-enzyme-electrode for continuous monitoring of glucose concentration in the isolated tubule preparation is described. The principle of the electrode is the amperometric detection of hydrogen peroxide, which is a product of the oxidation of D-glucose by glucose oxidase immobilized at the tip of a micro-electrode. The resulting current causes a voltage deflection across a resistor in series with the electrode that is correlated directly with the glucose concentration. The electrode response to glucose is almost linear over the concentration range from 0 to 12 mmol/l with a slightly diminished slope in the higher range. Other sugars (12 mmol/l raffinose, galactose, fructose, sucrose, mannitol), pH (from 6.5 to 8.0) and pCO2 (from 1 to 10 kPa) do not influence the reading. A reduction of pO2 in the test solution to 1 kPa blunts the reading. Raising the temperature from 20 degrees C to 40 degrees C leads to a pronounced increase of the voltage deflection at a given glucose concentration. Interference is observed with strongly reducing agents such as L-cysteine, ascorbic acid and uric acid. At defined conditions the electrode is well suited to measure continuously glucose concentration in the luminal fluid at the collection site of the isolated perfused tubule of the kidney. Experiments are presented which illustrate the performance of the glucose electrode in this isolated tubule set-up. Peritubular reduction of potassium concentration or the application of ouabain diminish glucose reabsorption.

Animals↗
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

Potassium transport in the early distal tubule of Amphiuma kidney. Effects of potassium adaptation.

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. Net K flux and electrochemical driving forces of K were described over a wide range of peritubular K concentrations. Whereas in control animals, at normal and low peritubular K concentrations K reabsorption occurs, K secretion is induced by elevating peritubular K. In contrast, net K secretion is seen at all peritubular K levels in the K-adapted kidney. Net K secretion approaches saturation at high peritubular K concentrations. Intracellular K activities also approach plateau values which are shifted upward in the state of K-adaptation. In control animals at zero net flux conditions intracellular K is maintained above electrochemical equilibrium across both the peritubular and the luminal cell membrane. After K-adaptation, however, K approaches electrochemical equilibrium across the luminal cell membrane. The results indicate that in control conditions, K is taken up actively into the cell across the peritubular and across the luminal cell barrier. It is likely that both luminal and peritubular transport components (increased luminal K conductance, diminished luminal K cotransport, stimulation of peritubular K-uptake) are responsible for increased K secretion during K adaptation.

Adaptation, Physiological↗
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

The effect of furosemide on luminal sodium, chloride and potassium transport in the early distal tubule of Amphiuma kidney. Effects of potassium adaptation.

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. In control animals the direction of net K transport is reversed from reabsorption to secretion upon addition of furosemide or following the removal of Cl from the tubular lumen. Volume reabsorption is inhibited by some 80%. In K adapted animals a similar inhibition of volume reabsorption is observed, however K secretion is not further enhanced. In control as well as in K-adapted animals intracellular K activities are still above electrochemical equilibrium after furosemide. The data suggest that a common transport system for Na, Cl and K is present in the luminal cell membrane which is inhibited by furosemide. K secretion observed in controls after furosemide and in K-adapted animals is driven by the cell to lumen electrochemical gradient for K across the K permeable luminal cell membrane. The shift of the luminal pump-leak system towards K secretion following K adaptation may be explained by an increase of the luminal K conductance and/or by a reduction of the activity of the luminal cotransport system. However, other mechanisms may also contribute to the observed phenomenon of K adaptation and cannot be ruled out at present.

Adaptation, Physiological↗
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↗