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F X Beck

Publications and source records attributed to F X Beck.

66 records · Page 4Linked to original sources
PubMed1987

Effect of potassium adaptation on the distribution of potassium, sodium and chloride across the apical membrane of renal tubular cells.

To assess the effect of K adaptation on the electrolyte concentrations of renal tubular cells and on the concentration gradients across the luminal membrane, electron microprobe analysis was employed on freeze-dried cryosections of the renal cortex and on freeze-dried samples of tubular fluid in control and high-K rats. The measurements were performed in individual cells of the proximal and superficial distal tubule and on samples of tubular fluid obtained by free flow micropuncture from proximal and early and late distal collection sites. The ingestion of a potassium-rich diet for at least 10 days together with an acute potassium load of 0.4 mmol/kg/h led to a small increase in potassium concentration of about 7 mmol/kg wet weight (w.w.) in all cell types analysed. In distal convoluted tubule, connecting tubule and principal cells sodium concentration was markedly decreased by 4, 4, and 6 mmol/kg w.w., respectively, while no significant changes in sodium concentration were found in proximal tubule and intercalated cells. No consistent changes in cell chloride could be observed under K adaptation. Analysis of the tubular fluid samples showed that the K concentration gradient across the apical cell membrane of all distal tubular cell types investigated was diminished in the high-K rats. The concentration gradient for sodium entry, however, was clearly enhanced in the distal convoluted tubule, connecting tubule and principal cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Intracellular ion concentrations in the frog cornea epithelium during stimulation and inhibition of Cl secretion.

The intracellular electrolyte concentrations in the isolated cornea of the American bullfrog were determined in thin freeze-dried cryosections using energy-dispersive X-ray microanalysis. Stimulation of Cl secretion by isoproterenol resulted in a significant increase in the intracellular Na concentration but did not change the intracellular Cl concentration. Similar results were obtained when Cl secretion was stimulated by the Ca ionophore A23187. Inhibition of Cl secretion by ouabain produced a large increase in the intracellular Na concentration and an equivalent fall in the K concentration. Again, no increase or decrease in the intracellular Cl concentration was detectable. Clamping of the transepithelial potential to +/- 50 mV resulted in parallel changes in the transepithelial current and intracellular Na concentration, but, with the exception of the outermost cell layer, in no changes of the Cl concentration. Only when Cl secretion was inhibited by bumetanide or furosemide, together with a decrease in the Na concentration, was a large fall in the Cl concentration observed. Application of loop diuretics also produced significant increases in the P concentration and dry weight, consistent with some shrinkage of the epithelial cells. The results suggest the existence of a potent regulatory mechanism which maintains a constant intracellular Cl concentration and, thereby, a constant epithelial cell volume. Through the operation of this system any variation in the apical Cl efflux is compensated for by an equal change in the rate of Cl uptake across the basolateral membrane. Cl uptake is sensitive to loop diuretics, directly coupled to an uptake of Na, and dependent on the Na and K concentration gradients across the basolateral membrane. Isoproterenol and A23187 seem to increase the Cl permeability of the apical membrane and thus stimulate Cl efflux. Ouabain inhibits Cl secretion by abolishing the driving Na concentration gradient for Cl uptake across the basolateral membrane.

Animals↗
PubMed1985

Cl transport in the frog cornea: an electron-microprobe analysis.

The intracellular electrolyte concentrations of the bullfrog corneal epithelium have been determined in thin freeze-dried cryosections using the technique of electron-microprobe analysis. Under control conditions, transepithelial potential short-circuited and either side of the cornea incubated in Conway's solution, the mean intracellular concentrations (in mmol/kg wet weight) were 8.0 for Na, 18.4 for Cl and 117.3 for K. These values are in good agreement with ion activities previously obtained by Reuss et al. (Am. J. Physiol. 244:C336-C347, 1983) under open-circuit conditions. From a comparison of the chemical concentrations and activities of Na and K a mean intracellular activity coefficient of 0.75 is calculated. For small ions no significant differences between nuclear and cytoplasmic concentration values were detectable. The Cl concentrations in the different epithelial layers were virtually identical and showed parallel changes at varying states of Cl secretion, suggesting that the epithelium represents a functional syncytium. For Na a concentration gradient between the outer and inner epithelial layer was observed, which can be accounted for by two different models of epithelial cooperation. The behavior of the intracellular Na and Cl concentrations after removal of Na, Cl or K from the outer or inner bathing medium provides support for a passive electrodiffusive Cl efflux across the apical membrane and a Na-coupled Cl uptake across the basolateral membrane. The results are inconclusive with regard to the exact mechanism of Cl uptake, indicating either a variable stoichiometry of the symporter or the presence of more than one transport system. Furthermore, a dependence of intracellular Cl on HCO3 and CO2 was observed. Extracellular measurements in corneal stroma demonstrated that ion concentrations in this space are in free equilibrium with the inner bath.

Animals↗
PubMed1985

Electron microprobe analysis of chloride secretion in the frog cornea.

Electron microprobe analysis was employed to measure the intracellular electrolyte concentrations of the bullfrog corneal epithelium. Under control conditions, transepithelial potential short-circuited and both sides of the isolated cornea incubated in Conway's solution, the mean intracellular concentrations were 8.0 for sodium, 18.4 for chloride and 117.3 for potassium (mmole/kg wet weight). These values are in good agreement with previously reported ion activities implying that the intracellular activity co-efficient for small ions is close to that of the extracellular space. No significant differences between the nuclear and cytoplasmic concentrations of small diffusible ions were detectable. Similarly, the chloride concentrations in the different epithelial layers were virtually identical and showed parallel changes at varying states of chloride secretion, suggesting that corneal epithelium represents a functional syncytium. The behavior of the intracellular ion concentrations after removal of sodium, chloride or potassium from the outer or inner bath is consistent with a passive electrodiffusive efflux of chloride across the outer membrane and a sodium coupled chloride uptake across the inner membrane. Furthermore, effects of bicarbonate and CO2 on the rate of chloride secretion and on the intracellular sodium and chloride concentrations were observed, indicating a possible role of pH in regulating chloride secretion.

Animals↗
PubMed1984

Intracellular electrolyte concentrations in the frog skin epithelium: effect of vasopressin and dependence on the Na concentration in the bathing media.

The intracellular electrolyte concentrations of the frog skin epithelium have been determined in thin freeze-dried cryosections using the technique of electron microprobe analysis. Stimulation of the transepithelial Na transport by arginine vasopressin (AVP) resulted in a marked increase in the Na concentration and a reciprocal drop in the K concentration in all epithelial cell layers. The effects of AVP were cancelled by addition of amiloride. It is concluded from these results that the primary mechanism by which AVP stimulates transepithelial Na transport is an increase in the Na permeability of the apical membrane. However, also some evidence has been obtained for an additional stimulatory effect of AVP on the Na pump. In mitochondria-rich cells and in gland cells no significant concentration changes were detected, supporting the view that these cells do not share in transepithelial Na transport. Furthermore, the dependence of the intracellular electrolyte concentrations upon the Na concentration in the outer and inner bathing solution was evaluated. Both in control and AVP-stimulated skins the intracellular Na concentration showed saturation already at low external Na concentrations, indicating that the self-inhibition of transepithelial Na transport is due to a reduction of the permeability of the apical membrane. After lowering the Na concentration in the internal bath frequently a Na increase in the outermost and a drop in the deeper epithelial layers was observed. It is concluded that partial uncoupling of the transport syncytium occurs, which may explain the inhibition of the transepithelial Na transport and blunting of the AVP response under this condition.

Amiloride↗
PubMed1983

Analysis of epithelial ion transport by X-ray microanalysis.

Energy dispersive X-ray microanalysis was employed to determine the intracellular electrolyte concentrations in various epithelial tissues. Analyses of the changes in the intracellular electrolyte concentrations during different functional states provided new insights into the mechanisms involved in transepithelial ion transport. Results obtained on the Na transporting frog skin epithelium confirmed the two-barrier concept of transepithelial Na transport involving a passive Na uptake and an active Na extrusion. The Na transport compartment comprises all living epithelial cell layers, only the outer cornified cells, the mitochondria-rich cells and gland cells being exceptions. Na influx across the outer barrier can be inhibited by amiloride or stimulated by novobiocin or vasopressin. In the Cl-secreting frog cornea the electrolyte concentrations in the various epithelial cell layers and cell types were almost identical, indicating that the epithelium forms a functional syncytium with regard to ion transport. Under virtually all experimental conditions the Cl concentration was found to be higher than the expected equilibrium values, favouring a passive exit from the cells towards the tear side. The results are consistent with the existence of a furosemide-sensitive coupled NaCl uptake process at the inner-facing cell membranes. In the rat kidney after K depletion a fall in cellular K by about 20% was observed both in proximal and distal tubular cells. Simultaneously a rise in the intracellular Na concentration was detected which, however, was insufficient to balance the loss in K. No significant differences could be detected between the various epithelial cell types which are thought to be involved in either K reabsorption or secretion. It is concluded that the fall in cellular K is not sufficient to explain the marked reduction in urinary K excretion during K depletion.

Animals↗
PubMedDate not supplied

Quantitative morphology of renal cortical structures during compensatory hypertrophy.

The compensatory hypertrophy in different renal cortical structures was studied in rats 10 and 21 days after unilateral nephrectomy (UNX). Quantitative morphological/stereological analysis revealed significant increases in total renal cortical volume--33% on day 10 and 48% on day 21--after UNX. These changes were paralleled by significant increments in the volumes of proximal convoluted tubule (PCT, 55%), distal convoluted tubule (DCT, 114%), and cortical collecting duct (CCD, 106%) segments on day 10. The corresponding changes on day 21 were 76, 122, and 212%, respectively. These alterations were accompanied by increases in segment length; 3% PCT, 23% DCT, and 50% CCD on day 10 and 9% PCT, 30% DCT, and 142% CCD on day 21 after UNX. The total luminal and basolateral cell membrane surface areas also exhibited a time-dependent increase after UNX. The increments in both luminal and basolateral membrane domains in PCT and DCT after 10 days were not significant, but reached significance after 21 days (PCT: luminal membrane 21%, basolateral membrane 63%; DCT: luminal membrane 98%, basolateral membrane 63%). In contrast, CCD membrane areas had increased substantially already 10 days after UNX (luminal membrane 92%, basolateral membrane 71%). It declined subsequently by day 21 (luminal membrane 57%, basolateral membrane 32%). The cell rubidium concentration after a 30-second rubidium infusion, an index of Na-K-ATPase activity, as well as sodium concentrations were unaltered in cells of all nephron segments investigated. Altogether the stereological analysis shows that the compensatory increase in organ volume can be attributed primarily to an increase in nephron epithelial volume. The PCT responds with 'radial' hypertrophy (thickening of the tubular epithelial wall), while the DCT undergoes 'length' hypertrophy (increase of tubular length without thickening of the tubular wall and without an increase in number of cells). This type of hypertrophy is especially prominent on day 21 after UNX for the CCD which doubles in length. Only on day 10 does the CCD seem to respond with hyperplasia. Adaptive changes in response to UNX develop gradually. Only a few of the morphological parameters studied had completed their change by 10 days, the majority required longer.

Adaptation, Physiological↗
PubMedDate not supplied

Cellular osmoregulation in renal medulla.

Cells of the renal medulla adapt osmotically to varying external electrolyte concentrations mainly by changing the intracellular content of small organic osmoeffectors (osmolytes) such as sorbitol, inositol and trimethylamines. This implies that despite extreme variations in extracellular tonicity the intracellular concentrations of monovalent electrolytes are stabilized at levels optimal for enzyme function and cell metabolism. In contrast to inorganic electrolytes these organic osmolytes are metabolically neutral and thus do not affect cell metabolism. In addition, some of these organic osmoeffectors, the trimethylamine compounds, are known to counteract the deleterious effects of high urea concentrations (prevailing in antidiuresis) on structure and function of cell proteins.

Animals↗
PubMedDate not supplied

Sodium and potassium ion transport accelerations in erythrocytes of DOC, DOC-salt, two-kidney, one clip, and spontaneously hypertensive rats. Role of hypokalemia and cell volume.

Sodium (Na+) and potassium (K+) transport by the furosemide-sensitive Na+-K+ transport system, the Na+-K+ pump, and the cation leak(s) were studied in erythrocytes from DOC-water, DOC-salt, two-kidney, one clip (Sprague-Dawley), and spontaneously hypertensive rats (Wistar-Kyoto). Rubidium (Rb+) was used as a tracer for K+. After 4 weeks of DOC-salt hypertension, inward K+ (Rb+) transport by the furosemide-sensitive system was increased threefold, and the inward Na+ leak and the red cell Na+ content were elevated by about 50%. The rise in cell Na+ accelerated K+ inward and Na+ outward transport by the Na+-K4 pump, DOC-water hypertension caused similar but less pronounced changes. In two-kidney, one clip hypertension, the Na+ leak and the Na+-K+ pump rates were slightly elevated, and furosemide-sensitive Rb+ uptake tended to be increased. In spontaneously hypertensive rats, furosemide-sensitive Rb+ uptake was accelerated by 50%. The marked hypokalemia in DOC-water and DOC-salt hypertension was associated with a slight loss of red cell K+ and an increase in mean cellular hemoglobin content (MCHC), indicative of cell shrinkage. Hypokalemia induced by dietary K+ deficiency caused alterations in red cell cation transport, content, and cell volume which were qualitatively similar but more pronounced than those seen in DOC-salt hypertension. Osmotic shrinkage in vitro induced a severalfold acceleration of furosemide-sensitive Rb+ uptake, similar to that observed in rat erythrocytes shrunken in vivo in K+-deficient states. It is concluded that the acceleration of furosemide-sensitive K+ (Rb+) transport in erythrocytes of mineralocorticoid hypertensive rats is largely caused by the hypokalemia and consecutive red cell K+ loss and shrinkage, respectively. Mean cellular hemoglobin content (MCHC) is thus a parameter that must be considered in studies on Na+ and K+ transport across the membrane of rat erythrocytes.

Animals↗