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Biomedical subjects

H Völkl

Publications and source records attributed to H Völkl.

At least 19 recordsLinked to original sources
PubMed1991

Hepatorenal reflex regulating kidney function.

In anesthetized male rats, infusion of glutamine (2 mumol/min) into the superior mesenteric vein at a rate known to induce liver cell swelling leads to marked decreases in renal glomerular filtration rate, renal para-aminohippurate clearance and urinary flow rate. Glutamine infused at identical rates into the jugular vein does not elicit any of these effects. The effect of glutamine is mimicked by serine but not by glutamate. Spinal transection, renal denervation or section of the vagal hepatic nerves abolishes the effect of mesenteric venous glutamine infusion. Mesenteric application of glucagon (1 ng/min) or of both glutamine and glucagon enhances glomerular filtration rate and urinary flow rate. Infusion of 1 ng/min glucagon through the jugular vein does not significantly alter glomerular filtration rate or urinary flow rate. The data disclose a powerful liver-borne mechanism regulating kidney function that is mediated by the hepatorenal innervation.

Animals↗
PubMed1991

Electrophysiology of ammonia transport in renal straight proximal tubules.

To test for electrogenic transport of ammonium ions in straight proximal renal tubules, isolated perfused tubules have been exposed to peritubular ammonium ions during continuous recording of cell membrane potential. As a result, 20 mmol/liter NH4+ leads to a rapid, reversible depolarization of the cell membrane by 9.0 +/- 0.3 mV (N = 86). This depolarization is not significantly affected by 10 mmol/liter barium or 0.1 mmol/liter amiloride on both sides of the epithelium, but is significantly blunted by omission of extracellular bicarbonate and CO2 (3.8 +/- 0.4 mV, N = 9), by 1 mmol/liter acetazolamide (4.3 +/- 0.3 mV, N = 11), by 1 mmol/liter peritubular amiloride (4.3 +/- 1.1 mV, N = 7), by 1 mmol/liter SITS (5.7 +/- 0.4 mV, N = 6), and by replacement of extracellular sodium with choline (4.7 +/- 0.5 mV, N = 8). In the presence of both amiloride (1 mmol/liter) and acetazolamide (1 mmol/liter) in the bath, the NH4+ induced depolarization is completely abolished. Furthermore, the combined omission of bicarbonate and addition of 10 mmol/liter barium eliminates the NH4+ induced depolarization. About 50% of the depolarization can be explained by enhanced electrogenic bicarbonate exit due to the intracellular alkalosis. The other 50% is explained by amiloride and barium sensitive electrogenic entry of NH4+ into the cell.

Acetazolamide↗
PubMed1990

Effect of potassium on cell volume regulation in renal straight proximal tubules.

The present study was designed to assess for the influence of extracellular potassium and of inhibitors of potassium transport on cell volume regulatory decrease in isolated perfused straight proximal tubules of the mouse kidney. Volume regulatory decrease is virtually unaffected when bath potassium concentration is elevated from 5 to 20 mmol/liter, and still persists, albeit significantly retarded, in the presence of the potassium channel blocker barium on both sides of the epithelium and during virtually complete dissipation of the transmembrane potassium gradient by increasing extracellular potassium concentration to 40 mmol/liter. As evident from electrophysiologic observations, barium blocks the potassium conductance of the basolateral cell membrane. Reduction of bicarbonate concentration and increase of H+ concentration in the bath solution cannot compensate for enhanced potassium concentration and cell volume regulatory decrease is not affected in the presence of the K/H exchange inhibitor omeprazole. Similarly cell volume regulatory decrease is not affected by ouabain. In conclusion, potassium movements through potassium channels in the basolateral cell membrane are important determinants of cell volume and may participate in cell volume regulatory decrease. However, a powerful component of cell volume regulatory decrease in straight proximal tubules of the mouse kidney is apparently independent of potassium conductive pathways, K/H exchange and Na+/K(+)-ATPase.

Animals↗
PubMed1989

Effect of furosemide, bumetanide and mannitol on intracranial pressure in experimental brain edema of the rat.

Loop diuretics interfere with NaCl-KCl cotransport, which operates not only in the kidney but as well in a variety of nonepithelial cells including neuronal and glial cells. In these cells loop diuretics are able to reduce cellular volume. The present study has been performed to establish, whether furosemide or bumetanide directly modify intracranial pressure in cytotoxic brain edema. To this end, water intoxication was induced in animals acutely nephrectomized, to exclude any consequences of renal effects. Neither furosemide nor bumetanide proved effective in reducing intracranial pressure. In contrast, infusion of hypertonic mannitol solution leads to a marked, rapid reduction of intracranial pressure. The observations rule out a direct action of loop diuretics on intracranial cells to reduce intracranial pressure in water intoxicated animals.

Animals↗
PubMed1989

[Marginal gaps of combined composite and glass ionomer cement fillings in different preparations in vitro].

In 34 extracted molars with class V cavities (coronal margin in the enamel, apical margin in the dentin) a shoulder or a shoulder with bevel were prepared on the apical aspect. The dentin was covered with glass ionomer cement (GIC) and after beveling the neighboring enamel composite material was applied on top with enamel etching. 24 other cavities filled with either composite or glass ionomer cement served as controls. The specimen were exposed to 2000 alternating thermal tests (1 min. at 8 degrees C, 1 min at 60 degrees C) and alternations of the filling margins were recorded quantitatively using replicas in the SEM. After the alternating thermal tests GIC controls showed statistically significant better margin in enamel and dentin with shoulder preparations alone than the combined or pure composite fillings. Combined fillings with beveled apical cavity margins were superior to shoulder preparations alone. Glass ionomer cement seems to be better for the treatment of class V cavities in terms of margin tightness than composite alone or in combination.

Composite Resins↗
PubMed1988

Effect of amiloride on cell volume regulation in renal straight proximal tubules.

Amiloride has been shown to impair cell volume regulatory decrease in amphiuma red cells. The present study has been performed to test for the influence of amiloride on volume regulatory decrease and electrical properties in isolated perfused mouse straight proximal tubules. Replacement of 40 mmol/l NaCl with 80 mmol/l mannitol in bath perfusate does not appreciably affect the cell volume or the potential difference across the basolateral cell membrane. Reduction of osmolarity by omission of mannitol leads to cell swelling by 16.7 +/- 0.7% (n = 7), followed by volume regulatory decrease to 107.2 +/- 1.2% (n = 7) of original cell volume within 2 min. 1 mmol/l amiloride (but not 0.1 mmol/l amiloride) in the bath depolarizes the basolateral cell membrane from -63 +/- 1 mV (n = 24) by +16 +/- 1 mV (n = 16), decreases the apparent potassium transference number from 0.69 +/- 0.02 (n = 5) to 0.36 +/- 0.05 (n = 5), and significantly impairs volume regulatory decrease without appreciably modifying cell volume in isotonic solutions. 1 mmol/l amiloride in the luminal perfusate leads to a slight hyperpolarization of the basolateral cell membrane but does not interfere with volume regulatory decrease. Reduction of bath osmolarity depolarizes the basolateral cell membrane within 30 s by +7.8 +/- 0.8 mV (n = 18) in the absence and by +18 +/- 2 mV (n = 8) in the presence of amiloride. In the presence of reduced bath osmolarity and amiloride the potassium transference number amounts to 0.36 +/- 0.04 (n = 8). The hyperpolarization following luminal application of amiloride is most likely due to inhibition of luminal sodium channels, whereas bath amiloride depolarizes the basolateral cell membrane by reduction of basolateral potassium selectivity. As in amphiuma red cells amiloride impairs volume regulatory decrease in proximal straight renal tubules.

Amiloride↗
PubMed1988

Electrophysiology of cell volume regulation in proximal tubules of the mouse kidney.

The present study has been designed to test for the influence of cell swelling on the potential difference and conductive properties of the basolateral cell membrane in isolated perfused proximal tubules. During control conditions the potential difference across the basolateral cell membrane (PDbl) is -65 +/- 1 mV (n = 74). Decrease of peritubular osmolarity by 80 mosmol/l depolarizes the basolateral cell membrane by +7.8 +/- 0.5 mV (n = 42). An increase of bath potassium concentration from 5 to 20 mmol/l depolarizes the basolateral cell membrane by +25 +/- 1 mV (n = 11), an increase of bath bicarbonate concentration from 20 to 60 mmol/l hyperpolarizes the basolateral cell membrane by -3.2 +/- 0.5 mV (n = 13). A decrease of bath chloride concentration from 79.6 to 27 mmol/l hyperpolarizes the basolateral cell membrane by -1.8 +/- 0.7 mV (n = 6). During reduced bath osmolarity, the influence of altered bath potassium concentration on PDbl is decreased (delta PDbl = +16 +/- 2 mV, n = 11), the influence of altered bicarbonate concentration on PDbl is increased (delta PDbl = -6.0 +/- 0.8 mV, n = 13), and the influence of altered bath chloride concentration on PDbl is unaffected (delta PDbl = -1.8 +/- 0.6 mV, n = 6). Barium depolarizes the basolateral cell membrane to -28 +/- 2 mV (n = 16). In the presence of 1 mmol/l barium, decrease of peritubular osmolarity by 80 mosmol/l leads to a transient hyperpolarization of the basolateral cell membrane by -5.9 +/- 0.5 mV (n = 16).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Ionic requirement for regulatory cell volume decrease in renal straight proximal tubules.

The present study has been performed to test for the ionic requirement of regulatory cell volume decrease in isolated perfused straight proximal tubules of the mouse kidney. Reduction of peritubular osmolarity from 308 mosmol/l to 228 mosmol/l leads within 0.5 min to cell swelling by 16 +/- 1% (n = 26) of original cell volume (Vo). Within 2 min cell volume (V2) approaches 105 +/- 1% of Vo (n = 26) despite continued exposure to hypotonic bath perfusate. Reexposure of the tubules to isotonic bath perfusate shrinks the cells to 94 +/- 1% of Vo (n = 25). Within 2 min from omission of extracellular bicarbonate and CO2 regulatory cell volume decrease is impaired (V2 = 114 +/- 1% of Vo, n = 14). Similarly, regulatory volume decrease is blunted upon prior removal of extracellular sodium (V2 = 115 +/- 2% of Vo, n = 12). In contrast, regulatory volume decrease is not affected by prior removal of extracellular chloride (V2 = 104 +/- 2% of Vo, n = 9). Regulatory volume decrease is impaired in the presence of 1 mmol/l potassium channel blocker barium (V2 = 120 +/- 4% of Vo, n = 7) and of 1 mmol/l carbonic anhydrase inhibitor acetazolamide (V2 = 111 +/- 2% of Vo, n = 16) but is preserved in the presence of 1 mumol/l chloride channel blocker NPPB (V2 = 105 +/- 2% of Vo, n = 11). In conclusion, regulatory cell volume decrease apparently depends on potassium and bicarbonate, but does not depend on chloride.

Animals↗
PubMed1987

Potassium conductance in straight proximal tubule cells of the mouse. Effect of barium, verapamil and quinidine.

The present study has been performed to test for the influence of verapamil and quinidine on the potential difference across the basolateral cell membrane (PDbl) and on the basolateral potassium conductance of isolated perfused segments of the mouse proximal tubule. PDbl was recorded continuously with conventional microelectrodes during rapid alterations of bath or luminal perfusate composition. The contribution of the basolateral potassium conductance to the conductance of both cell membranes (tk) was estimated from the effects of altered bath potassium concentration on PDbl. Under control conditions tk approaches 0.8, i.e. the basolateral cell membrane is mainly conductive to potassium. Neither quinidine nor verapamil affect PDbl at concentrations below 10 mumol/l. At higher concentrations both substances depolarize the basolateral cell membrane mimicking the effect of 1 mmol/l barium. In the presence of 0.1 mmol/l verapamil tk is virtually abolished at 5 to 10 mmol/l bath potassium concentration but is almost unaffected at bath potassium concentrations between 20 and 40 mmol/l. 1 mumol/l ionophore A-23187 does not change the depolarizing effect of 0.1 mmol/l verapamil on cell membrane potential. In the presence of 0.1 mmol/l quinidine, tk is reduced to some 50%, irrespective of the bath potassium concentration. It is concluded that the potassium conductance in straight proximal tubules is inhibited not only by barium but as well by high concentrations of verapamil and quinidine. The effect is probably direct and not related to alterations in the intracellular calcium activity.

Animals↗
PubMed1986

Effects of ouabain and temperature on cell membrane potentials in isolated perfused straight proximal tubules of the mouse kidney.

In isolated perfused segments of the mouse proximal tubule, the potential difference across the basolateral cell membrane (PDbl) was determined with conventional microelectrodes. Under control conditions with symmetrical solutions it amounted to -62 +/- 1 mV (n = 118). The potential difference across the epithelium (PDte) was -1.7 +/- 0.1 mV (n = 45). Transepithelial resistance amounted to 1.82 +/- 0.09 k omega cm (n = 28), corresponding to 11.4 +/- 0.6 omega cm2. Increasing bath potassium concentration from 5 to 20 mmol/l depolarized PDbl by +24 +/- 1 mV (n = 103), and PDte by +1.6 +/- 0.1 mV (n = 19). Thus, the basolateral cell membrane is preferably conductive to potassium. Rapid cooling of the bath perfusate from 38 degrees C to 10 degrees C led to a transient hyperpolarization of PDbl from -60 +/- 1 to -65 +/- 1 mV (n = 21) within 40 s followed by gradual depolarization by +18 +/- 1% (n = 14) within 5 min. The transepithelial resistance increased significantly from 1.78 +/- 0.11 k omega cm to 2.20 +/- 0.21 k omega cm (n = 15). Rapid rewarming of the bath to 38 degrees C caused a depolarization from -61 +/- 2 mV (n = 17) to -43 +/- 2 mV (n = 16) within 15 s followed by a repolarization to -59 +/- 2 mV (n = 10) within 40 s. Ouabain invariably depolarized PDbl. During both, sustained cooling or application of ouabain, the sensitivity of PDbl to bath potassium concentration decreased in parallel to PDbl pointing to a gradual decrease of potassium conductance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

Kinetics of L-proline reabsorption in rat kidney studied by continuous microperfusion.

Renal tubular reabsorption of 3H and 14C labelled L-proline was measured in vivo et situ by continuous microperfusion of single proximal tubules of the rat. The reabsorption is shown to be saturable. Passive diffusion plays a relatively small role in the reabsorption. A maximum possible permeability coefficient of 25 micrometers 2.s-1 for proline was calculated. Two transport systems were found, one with a small affinity and a high capacity, the other with a very high affinity and a small capacity. The following values were estimated. Jmax 1 = 2.6 +/- 0.28 (SEM) nmol.m-1.S-1 Km1 = 11.8 +/- 1.7 (SEM) mmol.1-1 Jmax 2 = 9.6 +/- 1.92 (SEM) pmol.m-1.s-1 Km2 = 29.3 +/- 7.8 (SEM) mumol.1-1. Whereas the first system reabsorbs the bulk of the filtered load, the activity of the second system explains the extremely small amount of proline found in the final urine. Diisopropylphosphorofluoridate--a specific inhibitor of dipeptidyl peptidase IV--decreases the reabsorption of L-proline and L-alanine but has no influence on the reabsorption of the basic amino acid L-arginine and the acidic amino acid L-glutamic acid. This result correlates with a recent speculation that dipeptidyl peptidase IV is involved in proline and alanine reabosrption.

Animals↗
PubMed1977

Amino acid reabsorption in the proximal tubule of rat kidney: stereospecificity and passive diffusion studied by continuous microperfusion.

Renal tubular reabsorption of glycine and of the L- and D-isomers of histidine, serine, phenyl-alanine, methionine, proline and cystine was investigated in vivo et situ by continuous microperfusion of single proximal convolutions of the rat kidney. In the case of glycine and the L-isomers, tubular reabsorption is saturable to a great extent. The D-amino acids are reabsorbed much more slowly than the respective L-forms. Furthermore in the case of methionine and perhaps also of proline, serine and phenylalanine, the fractional reabsorption decreases in the presence of high concentrations of the L-form. This indicates that the D-isomers also have a measurable affinity for the reabsorption mechanisms of the renal tubule. The very poor reabsorption of D-amino acids in the presence of their L-isomers indicates that simple passive diffusion plays only a relatively small role in tubular amino acid reabsorption. Permeability coefficients estimated from these findings are in the range from 1--5 X 10(-7) cm2 - s-1. These values are very similar to those found for other organic molecules of comparable molecular weights.

Amino Acids↗
PubMedDate not supplied

Cell volume regulation in renal cortical cells.

Both proximal renal tubule cells and cultured Madin-Darby canine kidney (MDCK) cells are capable of regulating their volume in hypotonic media. Regulatory cell volume decrease in proximal straight tubules is impaired by barium, amiloride and acetazolamide and depends on the presence of bicarbonate and of sodium, whereas it is unaffected by complete removal of extracellular chloride. The observations may point to parallel loss of potassium through potassium channels as well as of bicarbonate and sodium via a bicarbonate-sodium cotransport. Alternatively, potassium/hydrogen ion exchange or potassium bicarbonate cotransport could be involved. In MDCK cells, exposure to hypotonic media apparently leads to the activation of an anion channel, while potassium conductance is rather decreased. In both proximal tubules and MDCK cells, volume regulatory decrease is possibly triggered by leucotrienes, which may be released during cell swelling. Cell volume is altered in a variety of conditions even at isotonic extracellular fluid and cell volume-regulatory mechanisms are likely to participate in regulation of renal transepithelial transport.

Animals↗
PubMedDate not supplied

Volume-regulatory potassium release from isolated perfused rat kidney.

The present study has been performed to test for cell volume regulatory potassium release from the isolated perfused rat kidney exposed to hypotonic perfusate and for its sensitivity to potassium channel blocker barium and calcium channel blocker verapamil. Replacement of 25 mmol/l NaCl with 50 mmol/l mannitol has little effect on effluent potassium activity, whereas subsequent omission of mannitol from the perfusate leads to a transient increase of effluent potassium activity, reflecting volume regulatory potassium release. Barium (1 mmol/l) leads to a marked transient decrease of effluent potassium activity, pointing to net cellular uptake of potassium. Verapamil (1 mumol/l) leads to a slight decrease of effluent potassium activity. Both barium and verapamil virtually abolish the rapid, transient increase of effluent potassium activity upon exposure to hypotonic perfusates. Thus, the substances either block or markedly retard volume regulatory potassium release. The apparent renal vascular resistance is transiently increased by exposure to hypotonic perfusates and by barium, but is reduced by verapamil. Cell volume regulation of isolated perfused mouse straight proximal tubules is retarded but not abolished by verapamil (0.1 mmol/l). In conclusion, cellular potassium release from rat kidney can be determined by continuous measurement of effluent potassium activity. The volume regulatory potassium release and cell volume regulation are impaired by both barium and verapamil. The persisting cell volume regulation could be due either to slow potassium release and/or some mechanism independent of potassium.

Animals↗