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G Rumrich

Publications and source records attributed to G Rumrich.

At least 55 records · Page 3Linked to original sources
PubMed1982

Transport of inorganic and organic substances in the renal proximal tubule.

The transport through the epithelial cell layer of the renal proximal tubule proceeds in principle by passive paracellular and active transcellular transport. The active transcellular transport is mostly secondary active. This means it proceeds coupled with the flux of Na+ ions, whereby the transcellular gradient of sodium, created by the (Na+ + K+)-ATPase, located at the contraluminal cell side, provides the main driving force. Once in the cell the substances leave the other cell side by a Na+ -independent, but carrier-mediated transport system. Using microperfusion and electrophysiological techniques as well as brush border membrane vesicle preparation the Na+ -H+ countertransport and the Na+-cotransport of amino acids, phosphate, sulfate, thiosulfate, bile acids, aliphatic-aromatic monocarboxylic acids (lactate) and dicarboxylic acids was studied. Special emphasis will be given to the bidirectional transport of thiosulfate as well as to the specificity of the monocarboxylic acid and dicarboxylic acid transport system.

Bile Acids and Salts↗
PubMed1981

Sodium-coupled taurocholate transport in the proximal convolution of the rat kidney in vivo and in vitro.

Using the standing droplet technique in the renal proximal convolution and simultaneous microperfusion of the peritubular capillaries, the zero net flux transtubular concentration difference of taurocholate (DeltaC(TC-)) at 45 s was determined as a measure of active bile acid reabsorption in vivo. Starting with 0.1 mmol/liter taurocholate in both perfusates the control DeltaC(TC-) of 0.042 mmol/liter fell to 0.006 mmol/liter (P < 0.001) when the Na(+) concentration in the perfusates was reduced to zero. Removal of bicarbonate from the perfusates to alter pH had no influence on DeltaC(TC-). When glycocholate was added to the perfusates DeltaC(TC-) was decreased, while probenecid increased DeltaC(TC-). These observations were extended by studies performed with brush border membrane vesicles derived from renal cortex. The initial (20 s) uptake of 0.01 mmol/liter taurocholate in the presence of a Na(o) (+) > Na(i) (+) gradient was stimulated twofold compared with its uptake in the absence of a Na(+) gradient. Uptake of taurocholate was osmotically and temperature sensitive. Membranes preloaded with unlabeled glycocholate showed accelerated entry of labeled taurocholate (trans-stimulation) only in the presence of Na(+). Replacement of Na(+) in the media with K(+), Li(+), and choline(+) decreased initial taurocholate uptake by 49, 53, and 62%, respectively. Stimulation of taurocholate transport by cation gradient diffusion potentials was unlikely inasmuch as the addition of valinomycin under K(+) gradient conditions had no effect. A transmembrane pH gradient (pH(o) < pH(i)) did not influence initial uptake of taurocholate. Finally, in the presence of Na(+) taurocholate transport showed cis-inhibition with unlabeled bile acids and saturation kinetics with respect to increasing taurocholate concentrations. The micropuncture and vesicle data indicate that the net transport of taurocholate in the proximal tubule is the result of an electroneutral Na(+)-taurocholate cotransport across the brush border membrane.

Animals↗
PubMed1980

Active sulfate reabsorption in the proximal convolution of the rat kidney: specificity, Na+ and HCO3- dependence.

Using the standing droplet technique in the proximal convolution and simultaneous microperfusion of the peritubular capillaries, the decrease in luminal sulfate concentration with time and the zero net flux transtubular concentration difference of sulfate (delta CSO42-) at 45 s was determined - the latter being taken as a measure of the rate of active sulfate reabsorption. Starting with 0.5 mmol/l sulfate in both perfusates the delta CSO42- value of 0.35 mmol/l was approached exponentially with a half value time of 4.3 s. The delta CSO42- values in the early proximal and late proximal convolution did not deviate from each other. If the Na+ concentration in the perfusates was reduced, the delta CSO42- approached zero and extrapolated to a slightly negative value (Ci greater than Co). When 1 mmol/l ouabain was added to the perfusates delta CSO42- decreased by 66% (the latter experiments were performed in the golden hamster which is more sensitive to ouabain than the rat). 1 mmol/l thiosulfate diminished delta CSO42- by 68% and 1 mmol/l molybdate by 24%. Omitting or replacing bicarbonate by HEPES or glycodiazine reduced the sulfate reabsorption significantly, while acetazolamide (0.1 mmol/l) and increasing the CO2-pressure from 4.66 to 14.0 kPa (i.e. 5-15% CO2) had no effect. SITS 1 mmol/l had no effect on sulfate reabsorption. The data indicate that the sulfate reabsorption is driven by a Na+ gradient and inhibited by thiosulfate and molybdate, i.e. molecules which have a similar tetrahedral molecule structure. The sulfate reabsorption depends in an undefined manner on the presence of bicarbonate ions.

Absorption↗
PubMed1980

Bidirectional active transport of thiosulfate in the proximal convolution of the rat kidney.

Using the standing droplet method in the late proximal convolution and simultaneous microperfusion of the peritubular capillaries, the zero net flux transtubular concentration difference of thiosulfate at 45 s was determined, the latter being taken as a measure of active thiosulfate transport. Under control conditions, in the presence of Na+, near zero delta c values were observed. When 1 mmol/l carinamide or paraaminohippurate (PAH) were added to the perfusates significant reabsorptive delta c arose. However, when 7.5 mmol/l sulfate was added to the Na+ containing perfusates or when the perfusates were Na+-free secretory delta c values were observed. Tested under Na+-free conditions, the secretory delta c was not influenced by simultaneously present 5 mmol/l of SO2-4 but was diminished by 50 mmol/l SO2-4. PAH (1 mmol/l), carinamide (0.2 mmol/l) and probenecid (1 mmol/l) decreased the secretory delta c by 48, 65 and 48%, respectively. The PAH secretion was not influenced, when thiosulfate or sulfate up to 50 mmol/l was added to both perfusates. Under Na+-free conditions the delta c of thiosulfate in early loops of the proximal convolution is higher than in late loops, while for PAH this pattern is reversed. Taken together with the previously published inhibition of sulfate reabsorption by thiosulfate the data indicate 1. thiosulfate is reabsorved by the Na+-dependent sulfate transport system and 2. thiosulfate is simultaneously secreted by a carinamide-, probenecid- and PAH-sensitive secretory system. The secretory system might also be shared by sulfate. The thiosulfate net flux is the result of the difference in the activity of the counteracting transporters, located at the luminal and contraluminal cell side. Is it possible that the higher activity of the transporter at one cell side leads to a reversal of the flux through the transporter at the other cell side.

Animals↗
PubMed1978

Phosphate transport in the proximal convolution of the rat kidney. III. Effect of extracellular and intracellular pH.

Inorganic phosphate (Pi) transport was evaluated using the standing droplet method with simultaneous microperfusion of the peritubular capillaries. To evaluate rather small differences in Pi transport and to eliminate the influence of tubular heterogeneity, the technique of crossed paired samples was applied. 1. In chronic PTX rats changing the luminal or both luminal and peritubular pH by varying the HCO-3-concentration between 4 and 50 mmol/l at constant 5% CO2 had no influence on Pi transport. 2. If, however, bicarbonate was omitted from the perfusate and 2 mmol/l phosphate (pH 7.4) was the only buffer, Pi transport was decreased from the control. It was, however, further reduced when the perfusates were gased with 5% CO2 i.e. the starting pH was 5.6. 3. When the solutions contained HEPES buffer (25 mmol/l), Pi transport at pH 8 was much larger than at pH 6.0. 4. Raising the CO2 pressure from 35 to 70 mm Hg did not change the Pi transport when both perfusates had a HCO-3-concentration of 25 mmol/l. It reduced, however, the Pi transport, when the luminal perfusate had only 4 mmol/l bicarbonate. 5. Lowering the CO2 pressure from 38 to 7.6 mm Hg did hardly change the Pi transport when the luminal perfusate contained 4 mmol/l bicarbonate. It lowered, however, the Pi transport significantly when the luminal perfusate had 2k mmol/l bicarbonate. 6. Acetazolamide, 10-4M, lowered the Pi transport when the luminal perfusate contained 4 or 25 mmol/l bicarbonate. At 4 mmol/l luminal HCO-3, raising the pCO2 to 228 mmol/l depressed Pi transport even more. At 25 mmol/l luminal bicarbonate, raising the pCO2 from 38 to 114 mm Hg reversed the acetazolamide inhibition of the Pi transport almost completely. The data indicate that luminal acidosis and intracellular alkalosis inhibits the transtubular Pi transport. A shift of the intracellular pH to a more alkaline value seems to be responsible for the inhibition of Pi transport by acetazolamide, while omission of buffer from the perfusate inhibits Pi transport by effecting an acidic luminal pH.

Acetazolamide↗
PubMed1978

Phosphate transport in the proximal convolution of the rat kidney II. Effect of extracellular Ca2+ and application of the Ca2+ ionophore A 23187 in chronic PTX animals.

Proximal inorganic phosphate (Pi) transport was evaluated using the standing droplet method with simultaneous microperfusion of the peritubular blood capillaries. In chronic parathyroidectomized (PTX) rats addition of 3 micron of the Ca2+ ionophore A 23187 to the luminal perfusate had no effect on the Pi transport, although the isotonic fluid reabsorption was reduced by 20%. When the Ca2+ concentration in the perfusates was raised from 1.5mM to 3.0mM the the reabsorption did not change significantly. But when Ca2+ was omitted from the perfusates the Pi reabsorption dropped by 19%, and when 2mM EDTA were added to the perfusates Pi transport decreased by 35%. The influx of Pi from the interstitial space and from the cell into the phosphate-free luminal perfusate did not change, when the perfusates were Ca2+ -free, but it increased by 23% in the presence of 2mM EDTA. The data indicate that 1. a rise in intracellular Ca2+ above normal is not a factor which modifies "basal" Pi transport i.e. when Pi transport is independent of the action of parathyroid hormone. 2. A reduction of extracellular Ca2+ concentration from normal toward zero reduces Pi transport without changing the paracellular leak permeability for Pi. 3. With EDTA the the paracellular leak permeability for Pi is increased, thus causing an even greater reduction in net Pi transport than with Ca2+ -free solutions alone.

Animals↗
PubMed1977

Coupling between proximal tubular transport processes. Studies with ouabain, SITS and HCO3-free solutions.

The rate of active transport by the proximal renal tubule of amino acid (L-histidine), sugar (alpha-methyl-D-glycoside), H+ ions (glycodiazine), phosphate and para-aminohippurate was evaluated by measuring the zero net flux concentration difference (deltac) of these substances. In the case of calcium the electrochemical potential difference (delta + zF-CIdeltaphi/RT) was the criterion employed. The rate of isotonic Na+-absorption (JNa) was measured with the shrinking droplet method. The effect of ouabain on the transport of these substances was tested in the golden hamster and the effect of SITS (4-acetamido-4'isothiocyanatostilbene 2,2'-disulfonic acid) was observed in rats. Ouabain (1 mM) applied peritubularly incompletely inhibited JNa (80%), but in combination with acetazolamide (0.2 mM) the inhibition was almost complete (93%). In addition, ouabain inhibited the sodium coupled (secondary active) transport processes of L-histidine, alpha-methyl-D-glycoside, calcium and phosphate by more than 75%. It did not affect H+ (glycodiazine) transport and PAH transport was only slightly affected. When SITS (1 mM) was applied from both sides of the cell it inhibited H+ (glycodiazine) transport by 72% and reduced JNa by 38% when given from only the peritubular cell side. SITS (1 MM), however, had no significant affect on H+ secretion and sodium reabsorption if it was applied from only the luminal side. Furthermore it had no affect on the other transport processes tested, regardless of the cell side to which it was applied. When the HCO-3 buffer or physically related buffers were omitted from the perfusate the absorption of Na+ was reduced by 66%, phosphate by 44%, and L-histidine by 15%. All the other transport processes tested were not significantly affected. The data are consistent with the hypothesis that the active transport processes of histidine, alpha-methyl-D-glycoside and phosphate, which are located in the brush border, are driven by a sodium gradient which is abolished by ouabain. This may also apply to the Na+-Ca2+ countertransport located at the contraluminal cell side. The residual Na+ transport remaining in the presence of ouabain is likely to be passively driven by the continuing H+ transport which probably is driven directly by ATP. SITS seems to inhibit the exit step of HCO-3 from the cell and secondary to that, the luminal H+-Na+ exchange and consequently the Na+ reabsorption. In the absence of HCO-3 buffer in the perfusates the luminal H+-Na+ exchange seems to be affected and the pattern of inhibition of the other transport processes is almost the same as with SITS. The different effects on Pi reabsorption observed under these conditions might be explained by possible variations in intracellular pH.

Animals↗
PubMed1976

Active Ca2+ reabsorption in the proximal tubule of the rat kidney. Dependence on sodium- and buffer transport.

Using the stop flow microperfusion technique with simultaneous capillary perfusion the rate active Ca2+ reabsorption was evaluated by measuring the static head electrochemical potential difference as well as the permeability of the tubular wall for Ca2+ ions. Under control conditions the active Ca2+ transport was calculated to be 3.35 X 10(-13) mol/cm - s. It declined toward zero if the ambient Na+ was replaced by choline or lithium. Parallel experiments in the golden hamster showed that active Ca2+ transport, vanished completely if active Na+ transport was blocked by ouabain (1 mM). These data indicate that the active Ca2+ reabsorption from the proximal tubule depends on the active reabsorption of Na2+ presumably via a Na+-Ca2+ countertransport at the contraluminal cell membrane. The static head electrochemical potential difference of Ca2+ is the same in late and early proximal tubules. It is also not affected by the presence of acetazolamide (10(-4) M) by the absence of bicarbonate or glycodiazine buffer or by the absence or presence of phosphate (2 mM).

Acetazolamide↗
PubMed1976

Specificity of sugar transport across the brush border of the rat proximal tubule.

By chemical and electrical measurements the transport of 25 sugars in the proximal tubule of the rat kidney was investigated. The data gained reveal the following structural requirements for the D-glucose transport system in the renal brush border: A free OH in the D-gluco-configuration on C atom 2 is most important - OH in equatorial position of the chair Cl conformation -. A free OH on C-3 in the equatorial configuration is also essential. If the OH on C-4 turns from the equatorial to the axial configuration the transport is 50% reduced. The OH on C-6 may be missing if otherwise the D-glucose configuration is unchanged. But if in addition the position of OH in C-4 has changed the transport ceases. Furthermore the presence of a C-6 atom and of a ring structure is necessary.

Animals↗
PubMed1975

Renal proximal tubular buffer-(glycodiazine) transport. Inhomogeneity of local transport rate, dependence on sodium, effect of inhibitors and chronic adaptation.

Using the stop flow microperfusion technique with simultaneous capillary perfusion the secretory rate of H+ ions in the proximal tubule was evaluated by measuring the level flow reabsorption as well as the static head concentration difference of 3H labeled glycodiazine. At ambient glycodiazine concentration of 21 mmol/l the level flow reabsorption is in the same range as that of bicarbonate. In the early proximal loops the reabsorption is 20% greater than in the late proximal loops. The carbonic anhydrase inhibitors acetazolamide and 3,4-methylene-dioxyphenyl-sulfonamide (both 10(-4) M) as well as furosemide (10 (-3) M) inhibit the glycodiazine reabsorption 43%, 27% and 22% respectively. Thiocyanate (2-10(-2) M), however, exerted only an insignificant inhibition (12%). When Na+ in the ambient perfusion solutions was replaced by Li+ or choline+ the glycodiazine transport was strongly reduced. Ouabain (5-10(-2) M) inhibited too, but amiloride (10(-3) M) had no effect on glycodiazine transport. The glycodiazine transport was 28% reduced in metabolic alkalosis and to a smaller although significant extent (17%) in metabolic acidosis; it was unchanged in chronic hypercapnia. In chronic K+ depletion the glycodiazine reabsorption was accelerated by 12% only in the early proximal loops. Chronic parathyroidectomy as well as acute substitution with parathyroid hormone had no effect on the glycodiazine absorption. The main conclusions are: Proximal H+ transport proceeds with suitable buffers. Although independent of HCO3- and carbonic anhydrase, it could be partially inhibited by CA inhibitors. H+ transport is supposed to proceed as countertransport with Na+ ions. In chronic alkalosis the H+ transport is reduced.

Acid-Base Equilibrium↗
PubMed1975

Renal phosphate transport: inhomogeneity of local proximal transport rates and sodium dependence.

The standing droplet method has been used in combination with the peritibular perfusion of blood capillaries to determine the build up of transtubular concentration differences of phosphate (Piota) in the renal proximal convoluted tubule of parathyroidectomized rats. Electron probe analysis was used to estimate Piota. At zero time both the intraluminal and the contraluminal Piota concentration was 2 mM. The time dependent decrease of the intraluminal Piota concentration was approximately 4 times faster in the early than in the late proximal convoluted tubule. After 45 sec an intraluminal steady state concentration of 0.20 mM Piota was achieved in the early part. In the late part the intraluminal Piota concentration approached a steady statevalue of 0.54 mM at 123 sec. When sodium free solutions were used the intaluminal Piota concentration increased to 2.22 mM in the earlier and to 2.76 mM in the late part. The data indicate that in the proximal convoluted tubule 1. the rate of phosphate reabsorption is greater in the early part than in the later part, and 2. phospate reabsorption might occur as co-transport with Na+ ions.

Animals↗