Potassium channels in renal epithelial transport regulation.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to W Rehwald.
Explore the source record for details and available documents.
In proximal renal tubules of the frog kidney, stimulation of sodium-coupled transport leads to a depolarization of the peritubular cell membrane, followed by partial repolarization. These alterations of the potential difference across the peritubular cell membrane (PDpt) are in part the result of altered peritubular potassium conductance. The repolarization has been blunted by the phospholipase A2 inhibitor mepacrine, but not by the cyclooxygenase inhibitor indomethacin. In the present study the effect of mepacrine, indomethacin and the lipoxygenase inhibitor nordihydroguaiaretic acid on the electrical properties of proximal renal tubules has been tested in the presence and absence of stimulated sodium-coupled transport. In the absence of inhibitors, addition of 10 mmol/l phenylalanine to the luminal perfusate leads to a rapid depolarization and partial repolarization of the peritubular cell membrane, a decrease of the luminal cell membrane resistance (Ra) and a small increase of the cellular core resistance (Rc). Removal of phenylalanine leads to rapid hyperpolarization, increase of Ra and decline Rc. Mepacrine (100 mumols/l) depolarizes the cell membrane and increases the peritubular cell membrane resistance (Rb), Rc and the intracellular pH. In the presence of mepacrine, phenylalanine leads to a sustained depolarization and a transient decrease of Ra. Indomethacin (10 mumol/l) does not significantly modify PDpt, the lumped resistance of both cell membranes (Rm) or Rc in the presence or absence of phenylalanine. Nordihydroguaiaretic acid (50 mumols/l) does not alter significantly PDpt, Ra, Rb or Rc prior to phenylalanine.(ABSTRACT TRUNCATED AT 250 WORDS)
Measurements of the gross beta activity of snow samples from four Alpine glaciers contaminated by radioactive fallout from the Chernobyl nuclear accident and a gamma-spectrum analysis of selected samples are reported. The results are discussed with respect to possible risks to the population from using meltwater from these glaciers as drinking water.
Measurements of the gross-beta-activity and a gamma-spectrum analysis of radioactive fallout from Chernobyl distributed in vertical snow profiles on an Alpine glacier were carried out. Samples were collected in summer 1986 and in summer 1987. A displacement of isotopes to depths of approximately 6 m was observed. The mean activity per unit area amounts to 10.4 and 6.6 kBq m-2 for samples from 1986 and 1987, respectively, both values corrected to 1 May 1987. Isotopes with half-lives shorter than 110m Ag (250 days) could no longer be detected in 1987.
In proximal tubules of the frog kidney, stimulation of coupled transport of sodium with phenylalanine leads to depolarization of the cell membrane, followed by repolarization within a few minutes. The repolarization is due to a delayed increase of potassium conductance at the peritubular cell membrane. The present study was designed to test for the role of depolarization, of calmodulin and of arachidonic acid metabolites for the delayed increase of potassium conductance. To this end, the potential difference across the peritubular cell membrane of proximal convoluted tubules (PDpt) has been recorded continuously during exposure of the lumen to phenylalanine or during galvanic current injection into a neighbouring cell. During control conditions, PDpt averages -68.6 +/- 1.0 mV (n = 45). Phenylalanine leads to a depolarization of the peritubular cell membrane by +31.5 +/- 1.3 mV (n = 20), followed by a repolarization by -12.9 +/- 1.1 mV (n = 20) within 3 min. Injection of currents from 10 to 80 nAmps leads to a depolarization by +0.83 +/- 0.01 mV/nAmps which is again followed by repolarization. A linear correlation is observed between the magnitude of depolarization (dep) and repolarization (rep) within 3 min: rep (mV) = -(0.24 +/- 0.01) dep (mV) +(2.45 +/- 0.12) mV (r = 0.90). Thus, depolarization is capable to trigger delayed repolarization. The extent of repolarization is a function of the magnitude of depolarization. The possible involvement of calmodulin or arachidonic acid metabolites has been tested for by inducing sodium coupled transport in the presence of 100 mumol/l mepacrine, 10 mumol/l indomethacin or 10 mumol/l trifluoperazine.
In order to test for the contribution of intracellular potassium activity to the link of sodium/potassium-ATPase activity and potassium conductance, studies with conventional and potassium selective microelectrodes were performed on proximal tubules of the isolated perfused frog kidney. The peritubular transference number for potassium (tk), i.e., the contribution of peritubular slope potassium conductance to the slope conductance of the cell membranes (luminal and peritubular), was estimated from the influence of peritubular potassium concentration on the potential difference across the peritubular cell membrane (PDpt). During control conditions, PDpt is -65 +/- 1 mV, intracellular potassium activity (Ki) 57 +/- 2 mmol/l and tk 0.41 +/- 0.05. The resistance in parallel of the luminal and peritubular cell membranes (Rm) is 44 +/- 4 k omega cm, the resistance of the cellular cable (Rc) 137 +/- 13 M omega/cm. When the cells are exposed 10 min to potassium free perfusates (series I), PDpt increases by -28 +/- 3 mV within 2 min and then decreases gradually to approach the control value within 10 min. Ki decreases by 22 +/- 3 mmol/l and Rc increases by 35 +/- 10%. After a transient decrease, Rm increases by 36 +/- 9%. Readdition of peritubular potassium leads to a transient increase of PDpt, a gradual decrease of Rm and Rc as well as a gradual increase of Ki. tk recovers only slowly to approach 65 +/- 8% of control value within 3 and 79 +/- 10% within 6 min.(ABSTRACT TRUNCATED AT 250 WORDS)
To test for the effect of cyanide on frog proximal renal tubules the potential difference across the peritubular cell membrane (PDpt) has been recorded continuously before and during peritubular application of 1 mmol/l cyanide using conventional microelectrodes. Before application of cyanide PDpt amounts to -61.5 +/- 2.2 mV in the absence of luminal substrate. Cyanide depolarizes the peritubular cell membrane by +18.8 +/- 2.3 mV/10 min in the presence and by +4.5 +/- 0.9 mV/10 min in the absence of luminal substrate. The rapid depolarization of the cell membranes to addition of glucose to luminal perfusate is not significantly influenced by exposure to cyanide, whereas the influence of altered peritubular potassium concentration (from 3 to 9 mmol/l) is significantly reduced from +15.2 +/- 1.7 mV to +8.7 +/- 1.8 mV. Following exposure to cyanide the lumped resistance of the luminal and peritubular cell membranes increases significantly by 36 +/- 7%/6 min, and the cellular core resistance significantly by 14 +/- 6%/6 min. As a result, cyanide markedly decreases the peritubular potassium conductance, depolarizes the cell membranes and reduces the driving force for sodium coupled transport processes. Thus cyanide fully mimics the effects of ouabain, although cyanide in contrast to ouabain is expected to deplete the cells from ATP. In conclusion ATP/ADP is not likely to play a major role in the regulation of sodium coupled transport processes and peritubular potassium conductance in amphibian proximal tubules.
The present study was designed to further test for the role of peritubular potassium conductance in the repolarization of peritubular cell membrane during sustained stimulation of sodium coupled transport by phenylalanine. To this end the potential difference across the peritubular cell membrane (PDpt) has been recorded continuously, while 10 mmol/l phenylalanine (Phe) were added to the luminal perfusate, both in the presence or absence of peritubular or luminal barium (1 mmol/l). In the absence of phenylalanine and barium, PDpt amounts to -65.5 +/- 2.2 mV. Phe leads to a rapid depolarization of the peritubular cell membrane by +36.2 +/- 2.2 mV within 30 s, followed by an almost complete repolarization by -28.9 +/- 2.6 mV within 7 min. In the presence of barium in peritubular perfusate, the depolarization following Phe is +24.3 +/- 2.6 mV and the repolarization almost abolished (-4.3 +/- 0.9 mV). In the presence of barium in luminal perfusate, Phe leads to a depolarization by +35.7 +/- 2.4 mV followed by a repolarization of -17.0 +/- 3.2 mV within 7 min. It is concluded that the repolarization during sustained stimulation of sodium coupled transport is in large part due to alterations of peritubular potassium conductance.
Effects of sodium-coupled transport on intracellular electrolytes and electrical properties of proximal renal tubule cells are described in this review. Simultaneous with addition of substrate for sodium-coupled transport to luminal perfusates, both cell membranes depolarize. The luminal cell membrane depolarizes due to opening of sodium-cotransport pathways. The depolarization of the peritubular cell membrane during sodium-coupled transport is primarily due to a circular current reentering the lumen via the paracellular pathway. The depolarization leads to a transient decrease of basolateral potassium conductance that in turn amplifies the depolarization. However, within 5-10 min of continued exposure to substrate, potassium conductance increases again, and peritubular cell membrane repolarizes. During depolarization the driving force of peritubular bicarbonate exit is reduced. As a result net alkalinization of the cell prevails despite an increase of intracellular sodium activity, which reduces the driving force for the sodium-hydrogen ion exchanger and would thus have been expected to acidify the cell. No evidence is obtained for regulatory inhibition of sodium-coupled transport by intracellular sodium or calcium. Rather, luminal cotransport is altered by the change of driving forces.
Measurements of gross beta activity and 3H concentration of firn samples from different regions can be used to determine environmental contamination by radioactive fallout from nuclear weapons tests in the atmosphere since 1952. The exposure dose to the population due to radioactive fission products in the drinking water supply from glacierized areas is compared to maximum acceptable concentrations derived from ICRP annual limits of intake (ALI). It is shown that even from heavily contaminated layers the risk to the population is acceptable.
The design and application of a micro-plantinum electrode for continuous monitoring of reducing activity in the isolated tubule preparation is described. The electrodes response to H2O2 up to 0.1 mmol/l, to uric acid up to 0.3 mmol/l, ascorbic acid up to 1.0 mmol/l and cysteine up to 2.0 mmol/l is almost linear. The electrode is insensitive to extracellular ions, to changes of pH (5.5-8.0), CO2 (1-10%) and O2 (1-100%). The reading of the electrodes is almost doubled when the temperature is increased from 20-40 degrees C. When reducing substances are omitted from the perfusate for isolated perfused proximal tubules of the mouse, the reading is identical in perfusate and collected fluid, indicating that the tubular epithelium does not produce redox substances in sufficient amount to interfere with the electrode reading at flow rates approximately 10 nl/min. When the tubule is perfused with solutions containing 0.3 mmol/l uric acid, the uric acid concentration in the collected fluid is 0.16 +/- 0.01 mmol/l after a contact time of 1.36 +/- 0.1 S, revealing net uric acid reabsorption. Adding probenecid to the luminal perfusion fluid leads to a 37.5 +/- 1.0% increase of uric acid concentration in collected fluid, disclosing the inhibitory effect of probenecid on uric acid reabsorption. If 0.3 mmol/l uric acid is added to the bath, 0.017 +/- 0.002 mmol/l uric acid is detected in the luminal fluid. The entry of uric acid into the lumen is abolished by 10(-4) mol/l pyrazinamide.
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.
Explore the source record for details and available documents.
The share of erythema dose of global radiation (Der/G) shows significant diurnal and annual variations. This is the result of the dependence of the ratio Der/G on optical air mass. Maximum values of Der/G are found at times of low optical air mass, i.e., at noon and in summer, minimum values at sunrise and sunset hours as well as in winter. Another reason for the annual variation of the ratio Der/G is the changing amount of total atmospheric ozone. Therefore values of Der/G in fall are about 50% higher than in spring despite the same solar declination. Comparing measurements of erythema dose at two stations with different altitudes, a difference of 14% per 1,000 m is obtained.
It was tried to demonstrate the laser-test simultaneously great groups of persons and thus to divide them roughly into prospective emmetropes and different ametropes. For that an interference-phenomenon of laser-light on a screen is used to determine the refractive status. If the head is moved slowly in one direction, myopes register a movement of the interference-pattern in the contrary sense, hyperopes a movement in the same sense, while emmetropes do not recognize a direction of movement. The refractive status of 139 students was investigated. The results of the laser-test with a small group of 24 students were compared with the results of retinoscopia, in the course of which the laser-test proved to be very sensitive. In 86% of the cases laser correction and retinoscopic correction were identical within a variation of +/- 0.25 dpt. All ametropic patients were detected with great certainty. Even negligible, subjectively not perceptible ametropia could be detected. Thus it was shown, that only 60% of those, who have been found to be ametropic by the laser-test, really do need glasses or a better correction. For determination of astigmatism further experiments are necessary.