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Biomedical subjects

G Malnic

Publications and source records attributed to G Malnic.

At least 91 records · Page 5Linked to original sources
PubMed1977

Kinetics of luminal acidification in cortical tubules of the rat kidney.

1. Some kinetic aspects of renal tubular acidification were studied in proximal and distal tubules of the rat kidney by combining stationary microperfusion methods and continuous measurements of luminal pH changes of phosphate or bicarbonate buffers by means of antimony electrodes. The analysis included the measurement of steady-state pH, steady-state buffer concentrations and acidification half-times. From these data, net rates of tubular bicarbonate reabsorption and of H ion secretion were obtained since it was shown that the rate of phosphate acidification provides a realistic estimate of H ion secretion. 2. Experiments were performed in control rats, in animals undergoing metabolic acidosis or alkalosis and in control and acidotic rats receiving the carbonic anydrase inhibitor Diamox. 3. In all experiments, the rates of tubular bicarbonate reabsorption and of phosphate acidification (H ion secretion) were proportional to luminal buffer levels. The changes of luminal acid concentrations followed first-order kinetics. 4. Steady-state transepithelial pH differences were reduced in metabolic alkalosis and after diamox but augmented during metabolic acidosis. 5. Acidification half-times were prolonged in metabolic acidosis and after Diamox but remained similar to control levels in metabolic alkalosis. 6. From the observation that both bicarbonate reabsorption and phosphate acidification are similarly affected by these experimental manoeuvres, it is concluded that H ion secretion plays a key role in both transport processes.

Acid-Base Equilibrium↗
PubMed1977

Mechansims and components of renal tubular acidification.

1. Renal cortical tubules of control and acetazolamide infused rats were perfused with 100 mM phosphate buffer at pH 5-5. The rate of alkalinization was measured by means of antimony micro-electrodes and was used to compute passive H ion fluxes from lumen to blood across the proximal and distal tubular epithelium. 2. The importance of other ionic movements that might contribute to pH changes of luminal buffers (chloride inflow into the lumen and bicarbonate diffusion across the epithelium) was assessed but found to be minor. H ion movements accounted for the majority of the observed pH changes. 3. H ion permeability of the tubular wall was calculated from the measured H fluxes and transepithelial concentration differences. It was 1-10 cm/sec, several orders of magnitude larger than those for other ions. However, such values are compatible with the mobility of protons in a medium of structure water within the limiting membrane. 4. A kinetic analysis of the mechanism of movement of H ions across the renal tubule is presented on the basis of experiments in which acidification and alkalinization of luminal buffers was followed in stationary microperfusions. The data are compatible with a pump-leak system in the proximal tubule, and with a model with low H ion permeability and a gradient dependent pump in the distal tubule.

Acid-Base Equilibrium↗
PubMed1976

H in cortical peritubular capillaries of rat kidney.

The pH of peritubular capillaries was measured by means of antimony microelectrodes, during their perfusion with mammalian Ringer's solutions at different pH, in control and acetazolamide infused rats. In capillaries perfused with a solution more acid than blood, significant alkalinization was observed at increasing distances from the point of perfusion, while during perfusions with more alkaline solutions, acidification was observed. Plotting the pH change observed per micrometer of distance from the perfusion point against the pH of the perfusing solution, the pH in equilibrium with tubular cells was interpolated. A value of 7.51 +/- 0.01 was found for control rats, significantly higher than the mean arterial blood pH of this group, of 7.39. In acetazolamide infused rats an equilibrium pH of 7.44 +/- 0.02 was found, still higher than the blood pH of 7.34. The slope of these lines was significantly greater in control than in acetazolamide treated rats. This slope was shown to evaluate permeability to the ions responsible for acid-base balance. The present data suggest that peritubular alkalinization is reduced after carbonic anhydrase inhibition due to decreased peritubular permeability to the involved ions, which represents a further site of action of these inhibitors.

Acetazolamide↗
PubMed1976

Conductances, diffusion and streaming potentials in the rat proximal tubule.

1. Transtubular potential differences and specific resistances were measured in rat proximal tubules by means of single and double barrelled glass micro-electrodes. 2. Tip localization was made by observation of effective resistance changes measured with double barrelled micro-electrodes upon passage of oil droplets, and by perfusion with choline C1. 3. Mean early proximal p.d.s. of the order of -1 to -2 mV, and late values of +0-5 to +1mV were found. Mean specific resistances ranged from 12 to 15 omega cm2. 4. Diffusion potentials and single ion relative conductances were evaluated, perfusing the lumen with solutions differing only with respect to one salt concentration. Na and K conductances were similar and greater than those of C1. 5. Luminal and peritubular perfusions with hypotonic solutions showed the occurrence of streaming potentials in this structure suggesting the existence of pores lined with negative charges. The effective diameter of these pores appeared to be reduced by hypotonic perfusion, as evidenced by a significant increase in resistance, indicating that the main ion path across this structure is represented by intercellular spaces.

Animals↗
PubMed1975

Peritubular pH and PCO'2 in renal tubular acidification.

The influence of peritubular capillary pH and PCO'2 on renal tubular acidification was studied in rats by luminal and peritubular perfusion techniques. Luminal stopped-flow microperfusions were carried out with bicarbonate or alkaline phosphate solutions and luminal pH continuously measured by antimony micorelectrodes. Peritubular calpillary microperfusions were carried out with mammalian Ringer solution kept at different pH and PCO'2. The acidification process was assessed in terms of 1)maximal pH differences, 2)rates of pH change, and 3)rates of bicarbinate reabsorption or H'+ ion secretion. During peritubular perfusions at physiological pH and PCO'2 tubular acidifying capacity was maintained at near-normal levels. Perfusingcapillaries at high pH and low PCO'2, especially with bicarbonate Ringer, acidification was markedly depressed; it was moderately reduced at a peritubular pH of 5.6. At a capillary pH of 7.4, acidification was similiar at low and physiological PCO'2and enhanced at elevated PCO'2. Systemic respiratory acidosis enhanced acidification in the proximal tubule, but reduced it in distal segments.

Acid-Base Equilibrium↗
PubMed1975

Effect of nonelectrolytes and tonicity on hydrosmotic properties of toad bladder.

Water flow was measured gravimetrically in toad bladder sacs incubated in solutions of different ionic content. Substitution of Ringer's solution by isotonic and hypertonic nonelectrolyte solution increases water permeability markedly and depresses the effect of ADH on this structure. This effect is not reversible returning to Ringer after a preincubation for 3 hours in these solutions. It is also found, to a lesser extent, in Ringer made hypertonic with NaCl. Such effects are prominent when nonelectrolyte solutions are applied to the serosal medium; when applied to the mucosal side only, isotonic nonelectrolyte solutions do not induce alterations in water permeability, while the effect of hypertonic solutions is delayed. In nonelectrolyte solutions, the addition of calcium tends to normalize water permeability, but not ADH action. The addition of potassium has no effect on either function. On the other hand, a normal water permeability can be maintained when up to 50% of Ringer's solution is substituted by 400 mM mannitol. These findings indicate that an adequate ionic content of its bathing fluids is necessary for the preservation of the hydrosmotic function of the toad bladder, and that this epithelium appears to be more sensitive to electrolyte depletion via its serosal cell membrane than across the mucosal border.

Animals↗
PubMed1973

Kinetics of potassium transport across single distal tubules of rat kidney.

1. The transport of potassium across the distal tubular epithelium was studied in vivo in rats on a normal potassium intake and in rats in which distal tubular potassium secretion was either stimulated by potassium loading or the I.V. administration of a 5% sodium bicarbonate solution or in which potassium secretion was suppressed by dietary deprivation of potassium or sodium.2. (42)K was used to measure unidirectional fluxes across the luminal and peritubular cell membranes and to assess the magnitude of cellular potassium partaking in the transport process. This was accomplished by the simultaneous perfusion of the peritubular capillary network with (42)K-Ringer and of the distal tubular lumen with initially tracer-free solution. From the steady-state flux and the time course of tracer washout into the lumen after discontinuing the peritubular perfusion, unidirectional fluxes, rate coefficients of ion transfer and cellular transport pools could be measured.3. Transepithelial movement of potassium involves mixing with a variable cellular potassium transport pool. The latter is significantly elevated in conditions of enhanced distal tubular potassium secretion; cellular potassium labelling is reduced in conditions in which potassium secretion has been suppressed by potassium deprivation.4. Evidence is presented that changes in the peritubular transport pattern are primarily responsible for modifications of potassium translocation. Thus, stimulation of potassium secretion is associated with increased peritubular potassium uptake; a reduced potassium uptake across the peritubular cell membrane accounts for the fall in potassium secretion in potassium-depleted animals. Whereas passive entry of potassium across the peritubular membrane is augmented in potassium-loaded animals, the induction of metabolic alkalosis by the administration of 5% sodium bicarbonate stimulates active potassium uptake across the peritubular cell membrane. Sodium deprivation stimulates active reabsorptive transfer of potassium from the tubular lumen.

Alkalosis↗