Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal function was examined in rats given daily injections of gentamicin (100 to 150 mg/kg) for 10 to 14 days. Whole kidney inulin clearance fell and urine volume increased. Single nephron GFR of surface nephrons varied. Some nephrons had no filtration, some had low rates, and some had high rates. Abnormal renal tubular epithelial inulin permeability was demonstrated by microinjection. Micropuncture of individual nephrons early and later in their course demonstrated reduced fluid reabsorption along the proximal convoluted tubule of superficial nephrons. Rates of fluid delivery to the late proximal and distal tubule were elevated. The rate of fluid reabsorption in the superficial loop of Henle was increased. Maximal urine osmolality and papillary tissue content of urea was reduced. The polyuria, therefore, results from decreased fluid reabsorption by proximal tubules and, probably, by papillary collecting ducts. The decrease in proximal fluid reabsorption is probably secondary to impaired solute reabsorption. A decrease in collecting duct fluid absorption can be attributed to the observed decrease in papillary solute concentration.
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PMID:Cortical and papillary absorptive defects in gentamicin nephrotoxicity. 664 17

The renal medullary countercurrent system differentiates into its final segmental nephron function and geometry during perinatal development. The influence of these changes on the medullary longitudinal osmotic gradient cannot be evaluated by experimental studies. Therefore, a computation analysis using a differential equation model of the renal countercurrent system was applied to quantitate the effect of medullary architecture and solute transport on the concentration profiles for salt and urea in tubules (loop of Henle and collecting duct) and in the central core along the entire medulla during ontogeny. The results indicate that both the changing distribution of loop segments within the medulla and the increase in active salt transport of the individual thick ascending loop determine the magnitude and slope of the axial medullary solute gradients.
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PMID:Determinants of axial osmotic gradients in the differentiating countercurrent system. 669 14

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 X 1(-1); and osmolality, 2548 +/- 141 mOsm X kg-1. Electrolyte concentrations in the interstitial space were: sodium, 437 +/- 19; chloride, 438 +/- 20; and potassium, 35 +/- 2 mmoles X 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 X 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 X 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.
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PMID:Intra- and extracellular element concentrations of rat renal papilla in antidiuresis. 672 35

The effects of cortisol excess on kidney function were studied in 8 normal conscious dogs. Cortisol was given orally until polyuria developed. Cortisol excess decreased urine osmolality (from 897 +/- 76 to 186 +/- 36 mosm. kg-1) and increased urine production (from 0.7 +/- 0.1 to 9.3 +/- 2.4 ml kg-1. h-1). The glomerular filtration rate increased by 23 +/- 9 per cent. Sodium and potassium concentrations in plasma were decreased. 66 Per cent of the increase in urine production was due to the increase in free water clearance and 34 per cent to the increased urea excretion. Cortisol excess apparently caused polyuria by inhibition of the action of ADH in the collecting duct, resulting in a decreased water and urea reabsorption. The decreased urea reabsorption possibly causes a smaller urea recirculation in the renal medulla and hence a decrease in concentrating capacity.
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PMID:The influence of cortisol excess on kidney function in the dog. 673 Feb 86

The hypotheses of passive salt accumulation predict an enhancement of renal concentrating ability by urea. We tested this prediction in rabbits, a species whose nephons when studied in vitro show tansport properties that support these hypotheses. We used calm, unanesthetized, hydropenic, vasopressin-treated rabbits with intact kidneys fed a 16% protein diet, and we observed the effect of urea administration at two rates of solute excretion (60 and 190 microOsm/min . kg body wt; N = 10 and 5, respectively). After an i.v. mannitol infusion, when urea was infused, the i.v. solute excretion rate was unchanged, the changes in urine urea concentration were large (a change of 767 and 408 mumoles/ml), but only small and variable changes in urine osmolality occured (a change of 78 +/- 146, and 36 +/- 50 microOsm/g H20). In additional experiments, we removed the kidneys from antidiuretic, or urea- or mannitol-infused rabbits and measured the intrarenal distribution of sodium, potassium, urea, and chloride. When the urine urea level was greater than 400 mmoles, the urine-to-papilla ratios for urea were 1.6 to 3.6. This suggested that a low collecting duct permeability to urea could explain the absence of a marked enhancement of concentrating ability during urea administration. Further analysis, based on a model of inner medullary solute compartments, indicated that sodium chloride was the major (86%) osmotically active solute in the medullary central core of these rabbits and that it was not influenced by changes in urinary urea concentration. The results of tissue analysis were consonant with either active or passive sodium chloride reabsorption from the thin ascending limb of Henle's loop in these rabbits.
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PMID:Urea and renal concentrating ability in the rabbit. 677 Jan 67

During steady-state water or mannitol diuresis, the microcatheterization technique was used to study the handling of urea, fluid, sodium, potassium, and total solute along the length of the medullary collecting duct in anesthetized rats. During water diuresis, the remaining fraction of filtered urea increased along the collecting duct as indicated both by regression analysis of all samples and by comparison of paired data from the beginning and end of the duct [(TF/P)urea/In = 43.3 and 50.7%, respectively]. During mannitol diuresis, similar urea entry into the medullary collecting duct was observed, (TF/P)urea/In increasing from 60.7 to 66.5%. Comparison of collecting duct urea handling in proximal and distal segments (beginning to midzone and midzone to papillary tip) suggested that urea entry occurred to a greater extent in the distal portion of the medullary collecting duct. The results demonstrate urea secretion into the medullary collecting duct in diuretic states when urine flow is high and intratubular urea concentration low. Whether urea entry into the collecting duct is an active or passive process cannot be determined from this study, but comparison between urea concentrations in the papillary interstitial fluid and in the urine or tubular fluid raises the possibility of an active urea secretory mechanism in the collecting duct.
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PMID:Urea secretion in medullary collecting duct of the rat kidney during water and mannitol diuresis. 678 92

Five theoretical principles that follow from qualitative consideration of renal architecture and tubular permeabilities are proposed to explain the concentration of urine in the mammalian kidney. These are: 1) The medullary loop of the doubly folded S-shaped configuration of the nephron permits solute supplied by ascending Henle's limb (AHL) to extract water from descending Henle's limb (DHL) and collecting duct (CD). 2) The cortical loop allows the diluted AHL fluid to return to isotonicity with cortical plasma before returning to the medulla. 3) The folded vasa recta and surrounding interstitium (the central core) provide an expansion chamber for the performance of osmotic work and a mixing chamber for salt and urea. This mixing induces passive salt transport out of AHL. 4) Overall, the system acts as a solute cycling multiplier from the AHL to vascular core and the osmotically equilibrated DHL and CD. 5) The short-looped nephrons provide urea to drive salt transport out of AHL of long nephrons in the inner medulla.
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PMID:The renal concentrating mechanism: fundamental theoretical concepts. 684 Feb 88

Cortical kidney explants from newborn New Zealand rabbits were cultured in Dulbecco's minimum essential medium (DMEM) containing 10% fetal calf serum. Within 24 h the explants formed 'globular bodies' which were completely covered by a monolayered epithelium. The cells were differentiated and resembled collecting duct epithelium. By culturing the globular bodies in Dulbecco's MEM with D-valine instead of L-valine, a monolayer of collecting duct cells was obtained and used for control experiments. For analysis and identification of synthesized glycoproteins, the globular bodies were incubated with various labelled carbohydrates and amino acids, and then fractionated. Glycoproteins secreted into the culture medium were not detected. Cell-associated glycoproteins were found in crude membrane fractions and then extracted with Triton X-100 for column chromatography, SDS-polyacrylamide electrophoresis in 6 M urea, isoelectrofocusing, and two-dimensional electrophoresis. Two prominent glycoproteins containing galactose and glucosamine were synthesized during the spreading of the epithelium, with an apparent molecular weight of 150,000 and 85,000 (SDS-PAGE). The synthesized glycoproteins differ in their content of radioactive glycoprotein precursor and leucine. The 85,000 dalton monomer glycoprotein has an isoelectric point of 3.5 and was identified by two-dimensional electrophoresis.
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PMID:Glycoprotein synthesis of renal collecting duct epithelium cultured as globular bodies. 685 45

The relation between functional and structural renal changes induced by lithium was studied in rats during long-term treatment and after withdrawal of lithium. Administration of LiCl in the diet for up to 21 weeks caused marked polyuria associated with a significant lowering of renal concentrating ability assessed by dehydration and vasopressin tests. Plasma creatinine and plasma urea were not significantly changed by the treatment. Upon withdrawal of lithium water intake and concentrating ability were normalized within 4--8 weeks. Lithium caused focal light microscopic changes in the distal convoluted tubule and the collecting duct, consisting of nuclear and cellular polymorphism and, after prolonged treatment, dilatation of tubular lumens with tubular cell atrophy. These changes appeared later than the concentrating defect and persisted when lithium was withdrawn after prolonged treatment. No significant correlation was found between the degree of tubular changes and water intake or concentrating ability. It is concluded that the reversible diabetes insipidus induced by lithium in rats cannot be explained directly by the light microscopical changes observed in the distal part of the nephron, although the structural changes may be secondary to the polyuric state induced by lithium.
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PMID:Functional and structural changes in the rat kidney by long-term lithium treatment. 707 12

The aims of the present study were to examine the effects of urea and isotonic saline loads separately and together on urea handling in the medullary collecting duct and surface distal tubules of the rat kidney. Microcatheterization of the medullary collecting duct during isotonic saline diuresis (saline at 5% of body weight per hour, plasma urea 4.3 mM/L), showed an increase in the remaining fraction of filtered urea from 56.2% at the beginning (corticomedullary junction) to 68.5% at the end (papillary tip) of the medullary collecting duct (n = 17 paired samples in six rats, p less than 0.05). There was no change in the fraction of filtered urea along the medullary collecting duct during urea diuresis (plasma urea 87 mM/L, n = 15 paired samples in six rats) or during urea--saline diuresis (plasma urea 103 mM/L, n =32 paired samples in nine rats). Micropuncture of surface distal tubules in the same animals showed an increase in the fraction of filtered urea between end-distal samples and the beginning of the medullary collecting duct from 28.9 to 56.2% during isotonic saline diuresis (p less than 0.001), and from 53.6 to 75.3% during urea--saline diuresis (p less than 0.01), but no change during urea diuresis (63.6 to 60.0%, p = NS). Our conclusions are as follows. (1) Urea entry into the medullary collecting duct during steady-state diuresis occurs at low intratubular urea contractions (isotonic saline diuresis) but not at high concentrations (urea--saline diuresis and urea diuresis). (2) Urea entry between the surface distal tubule and the beginning of the medullary collecting duct occurs during saline diuresis (isotonic saline diuresis and urea--saline diuresis) but not urea diuresis. The latter finding suggests that isotonic saline loads affect urea transport differently in juxtamedullary nephrons compared to superficial nephrons.
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PMID:Urea handling by the distal tubule and collecting duct of the rat during urea--saline, isotonic saline, or urea diuresis. 708 62


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