Electrolyte composition of renal tubular cells in gentamicin nephrotoxicity

Electrolyte composition of renal tubular cells in gentamicin nephrotoxicity. The effect of long-term gentamicin administration on sodium, potassium, chloride and phosphorus concentrations was studied in individual rat renal tubular cells using electron microprobe analysis. Histological damage was apparent only in proximal tubular cells. The extent of damage was only mild after 7 days of gentamicin administration (60 mg/kg body wt/day) but much more pronounced after 10 days. GFR showed a progressive decline during gentamicin treatment. In non-necrotic proximal tubular cells, sodium was increased from 14.6 ± 0.3 (mean ± SEM) in controls to 20.6 ± 0.4 after 7 and 22.0 ± 0.8 mmol/kg wet wt after 10 days of gentamicin administration. Chloride concentration was higher only after 10 days (20.6 ± 0.6 vs. 17.3 ± 0.2 mmol/kg wet wt). Both cell potassium and phosphorus concentrations were diminished by 6 and 15, and by 8 and 25 mmol/kg wet wt after 7 and 10 days of treatment, respectively. In contrast, no major alterations in distal tubular cell electrolyte concentrations could be observed after either 7 or 10 days of gentamicin administration. As in proximal tubular cells, distal tubular cell phosphorus concentrations were, however, lowered by gentamicin treatment. These results clearly indicate that gentamicin exerts its main effect on proximal tubular cells. Decreased potassium and increased sodium and chloride concentrations were observed in proximal tubular cells exhibiting only mild histological damage prior to the onset of advanced tissue injury. Necrotic cells, on the other hand, showed widely variable intracellular electrolyte concentration patterns

Cell rubidium uptake: A method for studying functional heterogeneity in the nephron

Cell rubidium uptake: A method for studying functional heterogeneity in the nephron. Rubidium uptake into individual tubule cells of rat renal cortex as measured by energy-dispersive X-ray microanalysis on freeze dried cryosections was used as an index of potassium transport. Over a 30 second period following intravenous infusion of rubidium (0.5 mmol/kg body wt) rubidium content increased in all cells. After 30 seconds, rubidium contents were (in mmol/kg dry wt): 225 ± 8 in distal convoluted tubule cells, 156 ± 7 in connecting tubule cells, 110 ± 7 in principal cells, 86 ± 4 in proximal tubule cells and 24 ± 2 in intercalated cells (mean ± SEM). When distal sodium and potassium transport were stimulated by hypertonic saline loading, rubidium uptake was selectively increased into distal convoluted tubule cells by 38%, into connecting tubule cells by 36%, and into principal cells by 52%. However, rubidium uptake into proximal tubule and into intercalated cells remained unchanged. The preferential uptake of rubidium into distal convoluted tubule cells, connecting tubule cells, and principal cells correlates well with the known transport functions of sodium and potassium, whereas intercalated cells are distinguished by low sodium and potassium transport activity

Intra- and extracellular element concentrations of rat renal papilla in antidiuresis

AbstractIntra- and extracellular element concentrations of rat renal papilla in antidiuresis. The element concentrations in various intra- and extracellular compartments of the tip of the rat renal papilla were determined during antidiuresis using electron microprobe analysis. Urinary concentrations (means ±SEM) were: urea, 1509 ± 116; potassium, 268 ± 32; sodium, 62 ± 19 mmoles · 1-1; and osmolality, 2548 ± 141mOsm · kg-1. Electrolyte concentrations in the interstitial space were: sodium, 437 ± 19; chloride, 438 ± 20; and potassium, 35 ± 2mmoles · kg-1 wet wt. The vasa recta plasma exhibited almost identical element concentrations. The values in the papillary collecting duct cells were: sodium, 28 ± 1; chloride, 76 ± 3; potassium, 135 ± 3; and phosphorus, 316 ± 7 mmoles · kg-1 wet wt. Similar concentrations were observed in the papillary epithelial cells. In interstitial cells potassium and phosphorus concentrations were virtually identical to those of the collecting duct cells, whereas sodium and chloride concentrations were higher by about 30 mmoles · kg-1 wet wt. The element composition of the various papillary cells is, thus, not substantially different from that of proximal tubular cells. This finding demonstrates that cellular accumulation of electrolytes is not the regulatory mechanism by which papillary cells adapt osmotically to their high environmental osmolality and sodium chloride concentration.Concentrations élémentaires intra- et extra-cellulaires dans la papille rénale de rats en antidiurèse. Les concentrations élémentaires dans les différents compartiments intra- et extra-cellulaires de la pointe de la papille rénale de rats ont été déterminées pendant une antidiurèse, en utilisant une analyse à la microsonde électronique. Les concentrations urinaires (moyenne ±SEM) étaient: urée, 1,509 ± 116; potassium, 268 ± 32; sodium, 62 ± 19 mmoles-1; et l'osmolalité de 2,548 ± 141 mOsm · kg-1. Les concentrations d'électrolytes dans l'espace interstitiel étaient: sodium, 437 ± 19; chlore, 438 ± 20; et potassium, 35 ± 2 mmoles · kg-1 de tissu sec. Le plasma des vasa recta avait des concentrations élémentaires pratiquement identiques. Les valeurs dans les cellules du canal collecteur papillaire étaient: sodium, 28 ± 1; chlore, 76 ± 3; potassium, 135 ± 3; et phosphore, 316 ± 7 mmoles · kg-1 de tissu humide. Des concentrations identiques ont été observées dans les cellules épithéliales papillaires. Dans les cellules interstitielles, les concentrations de potassium et de phosphore étaient virtuellement identiques à celles des cellules du canal collecteur, tandis que les concentrations de sodium et de chlore étaient plus élevées d'environ 30 mmoles · kg-1 de tissu humide. La composition élémentaire des différentes cellules papillaires n'est, ainsi, pas substantiellement différente de celle des cellules tubulaires proximales. Ce résultat démontre que l'accumulation cellulaire d'électrolytes n'est pas le mécanisme de régulation par lequel les cellules papillaires s'adaptent osmotiquement à une osmolalité et à une concentration de chlorure de sodium ambiantes élevées