Urinary sodium, potassium, chloride, calcium, magnesium, phosphate, urate and urea in healthy subjects aged 5-18 years.
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The innate susceptibility of renal cell types to these agents was investigated using precision-cut rabbit renal cortical slices made perpendicular to the cortical-papillary axis. Slices were incubated in DME/F12 medium containing 10 microM, 100 microM, or 1 mM concentrations of either metal for 12 hr or in Krebs-Hepes buffer gassed with nitrogen (100%) for 0.75 to 5 hr of hypoxic exposure. To simulate postischemic reperfusion, some slices were transferred to vessels gassed with oxygen after an initial hypoxic period. Mercuric chloride (100 microM) exposure resulted in damage to the straight regions of proximal tubules by 12 hr leaving convoluted regions unaffected. Hypoxia (2.25 hr) and potassium dichromate (100 microM for 12 hr) both caused injury to the convoluted proximal tubules without affecting straight proximal tubular regions. Mercury concentrations of 10 microM and 1 mM had no effect or injured all cell types within the slice, respectively. Similar results were observed for hypoxic periods less than 1.5 hr or greater than 3 hr of exposure. Potassium dichromate had no measurable affect at 10 microM, but at 1 mM focal lesions were observed after 4 hr of exposure, and by 12 hr all cell types within the slice were affected. Intracellular potassium content normalized to DNA correlated well, but always preceded the pathological lesions observed. These results demonstrate that injury to specific regions of the proximal tubule by these agents relates to an innate susceptibility of the intoxicated cell type independent of physiologic feedback or blood delivery patterns proposed as mechanisms of selective injury from in vivo studies.
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Furosemide-inhibitable K influx is threefold higher in resealed ghosts of human erythrocytes than in intact cells. The enhancement is specific for K in that furosemide-inhibitable Na influx is the same in resealed ghosts and intact cells. The enhanced K influx resembles K-Cl cotransport in intact cells in that it requires Cl but not Na. N-ethylmaleimide (NEM), which stimulates furosemide-inhibitable K influx in intact cells, is without effect (or slightly inhibitory) in resealed ghosts. The failure of NEM to enhance the flux was not due to low ATP in the ghosts. These findings suggest that enhancement of the K flux in ghosts occurs by oxidation of membrane protein sulfhydryl groups, known to occur with lysis, the same sulfhydryl groups at which NEM acts by alkylation. This conclusion is supported by two observations: dithiothreitol completely prevents the increase in K influx in ghosts; this agent inhibits both oxidation of sulfhydryl groups and alkylation of them by NEM; and K influx in resealed ghosts is sensitive to changes in cell volume, just as it is in NEM-treated intact cells.
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According to Davis' (1965) model of the inner ear, a potential difference between the endocochlear potential and the hair cell resting potential drives the transduction current across the apical hair cell membrane. It is assumed that the endocochlear potential (EP) consists of two components. The first is a diffusion potential, which depends on the ionic composition of endolymph and perilymph and on the permeability of the perilymph-endolymph barrier. The second is an electrogenic component which is determined by active ion transport across the perilymph-endolymph barrier. In birds, the EP is between +8 and +20 mV. Little is known about the underlying mechanisms responsible for the measured EP in birds. The present paper studies whether ionic compositions of endo- and perilymph might explain the EP in birds. Concentrations of Na+, K+, Ca2+ and Cl- in pigeon scala vestibuli, scala tympani and scala media were determined with ion-selective microelectrodes. Na+, K+, Ca2+ and Cl- were 150.0, 4.2, 1.4 and 117.0 mM in perilymph (scala tympani and scala vestibuli). In scala media, the concentrations of K+, Ca2+ and Cl- were 140.6, 0.23 and 142.1 mM.
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