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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mathematical model of the nephron was developed by writing a set of material balance equations for the flow of urea, salt and water along the foregoing study and are taken here as a basis, in particular the model configuration of the collecting duct system. The stimulation of the model equatentration profiles which at the ends of the several tubular sections were consistent with the values observed in experimental investigations.e medullary interstitial solute concentration profiles are taken to increase linearly in outer and inner zone. The several transeptithelial fluxes are driven by diffusion, osmosis, solvent drag and active transport. The development of osmotic gradient in the inner medulla is taken here to be caused by active secretion of salt into the descending LImb of Henle's loop. The parameters in the flux equations for all parts of the nephron and the concentration values at the end of each tubular section are determined by collecting and averaging the values given in literature and by extrapolating the measurement data. The simulation of the model equations with these averaged parameters resulted in concentration profiles which at the ends of the several tubular sections were consistent with the values observed in experimental investigations.
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PMID:A functional model of the rat kidney. 42 7

Micropuncture techniques were employed to evaluate the effects of unilateral ureteral obstruction (UUO) of 18 h duration on the function of the terminal collecting duct in weanling rats 90-120 min following release of obstruction. In control animals and after release of UUO, water and sodium reabsorption continued along the terminal segment of the collecting duct. Fractional delivery of water (FRH2O) and sodium (FRNa) to this segment was increased after release of UUO. A significantly greater amount of the FRH2O and FRNa was reabsorbed along the terminal collecting duct following release of obstruction than in controls. Potassium was not consistently reabsorbed or secreted in either group. Following release of UUO, the osmolality of collecting duct fluid was lower than in controls, but was not different from the osmolality of fluid obtained from the bend of the loop of Henle. The results suggest that the permeability to water and the reabsorptive capacity of the collecting duct are not altered by acute obstruction.
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PMID:Effect of acute ureteral obstruction on terminal collecting duct function in the weanling rat. 42 68

Juxtamedullary (JM) nephron and collecting duct function was studied after a two-thirds reduction in renal mass in the young rat. The glomerular filtration rate of JM nephrons was twofold greater in the remnant kidney (RK) group than in controls, but this increase was proportional to the increase measured in surface nephrons. Despite an increase in absolute reabsorption, delivery of sodium and water to the end of the proximal tubule of superficial nephrons and to the bend of Henle's loop of JM nephrons was increased. This was a consequence of an increase in filtered load and a decrease in fractional reabsorption. Potassium handling in surface nephrons was similar to that of sodium and water. In deep nephrons of the RK group, potassium delivery to the bend was increased as a consequence of increased filtered load. The terminal portion of the collecting duct has a role in this adaptive response to a reduction in renal mass. In rats with a RK, reabsorption of water occurred along this segment; however, when the amount reabsorbed was related to delivery, fractional water reabsorption was only 30% of controls. Changes in sodium handling were more profound. In the group with the RK, sodium reabsorption was not detectable along this segment. Thus, while 40% of delivered sodium was reabsorbed in controls, in the remnant kidney group the mean was not different from zero (-1.7%).
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PMID:Response of deep nephrons and the terminal collecting duct to a reduction in renal mass. 44 83

We characterized renal tubular reabsorption before and during acute expansion in anesthetized 12-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Although mean arterial pressure was higher in euvolemic, nondiuretic SHR than in WKY, 158 vs. 114 mmHg, kidney and nephron glomerular filtration rate (GFR) as well as fluid reabsorption by the proximal convoluted tubule, loop of Henle, and distal convoluted tubule-collecting duct were similar. In euvolemic SHR with aortic constriction (SHR-AC), an acute decrease in renal perfusion pressure to 114 mmHg reduced sodium and water excretion. Kidney and nephron GFR and fluid reabsorption by segments along the nephron resembled values for SHR and WKY. Infusion of isotonic saline (3 ml.100 g body wt-1.h-1) produced similar increases in fractional sodium and water excretion by SHR and WKY, whereas SHR-AC exhibited a blunted natriuresis and diuresis. During expansion, fluid reabsorption by the nephron segments did not differ appreciably among the three groups. The effect(s) of perfusion pressure on reabsorption by superficial nephrons may be covert and was not unmasked, or may be manifested preferentially by deeper nephrons. We conclude that kidneys of SHR require a higher arterial pressure than kidneys of WKY to excrete a given amount of salt and water.
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PMID:Renal tubular reabsorption in spontaneously hypertensive rats. 46 59

The renal pelvis of the hamster has been studied by light microscopy (epoxy resin sections), transmission electron microscopy, and morphometric analysis of electron micrographs. Three morphologically distinct epithelia line the pelvis, and each covers a different zone of the kidney. A thin epithelium covering the outer medulla (OM) consists of two cell types: (1) granular cells are most numerous and have apically positioned granules which stain intensely with toluidine blue, are membrane-bound, and contain a fine particulate matter that stains light grey to black in electron micrographs. (2) Basal cells do not have granules, are confined to the basal lamina region, and do not reach the mucosal epithelial surface. The inner medulla (IM) is covered by a pelvic epithelium morphologically similar to collecting duct epithelium of IM. Some cells in this portion of the pelvic epithelium (IM) stain intensely dark with toluidine blue, osmium tetroxide, lead, and uranyl acetate. Transitional epithelium, which separates cortex (C) from pelvic urine, has an asymmetric luminal plasma membrane and discoid vesicles, each of which is similar to those previously observed in mammalian ureter and urinary bladder epithelia. Based on morphological comparisons with other epithelia, the IM and OM pelvic epithelia would appear permeable to solutes and/or water, while the transitional epithelium covering the C appears relatively impermeable. It would also appear that the exchange of solutes and water between pelvic urine and OM would involve capillaries, primarily, since morphometric analysis showed that both fenestrated and continuous capillaries of the OM were extremely abundant (greater than 60% of OM pelvic surface area) just under the thin pelvic epithelium.
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PMID:Ultrastructural organization of the hamster renal pelvis. 48 9

Antidiuretic hormone (ADH) administration to a polyuric Miniature Poodle did not alter diuresis. Plasma ADH concentrations were high, and urine osmolality remained low during water deprivation. From these findings, it was concluded that the polyuria was of renal origin. In addition, the glomerular filtration rate was found to be high. Electron microscopic examination of the renal medulla revealed vacuoles containing myelinic figures and fingerprint structures in the cells of the Henle loops, blood vessels, and interstitium, similar to those in lysosomal lipid storage disease. Their absence in collecting duct epithelium indicated that the defect in concentrating ability was due to a disturbance of the counter-current multiplier mechanism rather than to a defect in ADH receptors.
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PMID:Nephrogenic diabetes insipidus in a dog with renal medullary lesions. 50 Apr 24

The functional expression of papillary necrosis was investigated with a model of drug-induced papillary necrosis. Bromoethylamine hydrobromide (BEA) administration to rats uniformly resulted in the development of papillary necrosis. All studies were performed 24 hours after BEA administration with the exception of the electrolyte balance studies, which were performed during the 72 hours after the induction of papillary necrosis. GFR was not different between BEA-treated and sham rats. BEA-treated rats had a significantly lower maximal urine osmolality and free water reabsorption than did sham rats. Renal tissue concentrations of sodium, potassium, and water were not different between BEA-treated and sham rats. During water diuresis, free water clearance was not significantly different between the two groups. During sodium bicarbonate administration, maximal bicarbonate reabsorption and urine-blood Pco2 gradient (at comparable urine bicarbonate concentrations) were not significantly different between the two groups. During sodium sulfate infusion, there was no difference in minimum urine pH, ammonium excretion, and net acid excretion between chronically acidotic BEA-injected and sham rats. In rats on "zero" sodium intake, BEA administration resulted in a significant increase in urine flow and sodium excretion, whereas sham rats remained in sodium balance. In rats with restriction of both sodium and chloride, BEA administration resulted in a significant wastage of sodium, chloride, and calcium. There was no difference in potassium excretion between BEA-treated and sham rats during hydropenia, bicarbonate administration, sodium sulfate infusion, or ingestion of a normal potassium diet. When potassium intake was restricted to "zero," BEA-treated rats developed potassium wastage; when potassium intake was increased to 21 mEq/day, BEA-treated rats had a significantly lower potassium excretion than did sham rats. These findings may result from alterations in collecting duct transport, but damage to deep medullary structures may also contribute.
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PMID:Functional characterization of drug-induced experimental papillary necrosis. 51 89

The dive was carried out in the open sea to a depth of 850 fsw (26.7 ATA) for 6 days (DD 1--6) in the saturated mode, with personnel transfer capsule (PTC) excursions between 0 and 150 fsw and diver excursions between 0 and 50 fsw from the saturation base. Each diver had two excursion dives on alternate days. Although each PTC excursion lasted approximately 7 h, the actual time spent in the water averaged 10.5 min per diver. For 12 divers, daily excretion of water, electrolytes, aldosterone, and antidiuretic hormone (ADH) was studied, along with plasma composition (including prolactin), before, during, and after hyperbaric exposure. A significant increase in urine flow was observed on DD2--4 (1604 ml/day predive vs. 2300 ml/day on DD 4; P less than 0.05), after which the degree of diuresis decreased to about 1800 ml/day. Urine osmolality changed inversely with urine flow, with the lowest value of 532 mOsm/kg on DD 4. During the postdive period, both urine flow and urine osmolality returned to the predive level. The endogenous creatinine clearance was maintained at about 200 liters/day throughout the dive. The fractional excretion of Na+ remained unchanged while that of K+ increased significantly during hyperbaric exposure, thus decreasing the urinary Na+/K+ ratio. The fractional excretion of total osmotic substances showed a small hyperbaric exposure. Body weight decreased progressively during the initial 4 days of pressure exposure, equalling 2.6 kg on DD 4. These findings suggest that the observed diuresis may be accompanied by a net loss of body water. Neither the plasma prolactin level nor urinary excretion of aldosterone and ADHshowed any consistent change throughout the dive. It thus appears that, although there is a small osmotic component, the observed diuresis is primarily due to the ADH-independent inhibition of fre water reabsorption from the collecting duct by means of a mechanism yet to be identified.
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PMID:Urinary excretion of water and electrolytes during open-sea saturation diving to 850 fsw. 52 29

The renal reabsorption of water independent of solute is the result of the coordinated function of the collecting duct and the ascending limb of the loop of Henle. The unique juxtaposition of the ascending and descending portions of the loop of Henle and of the vasa recta permits the function of a counter-current multiplier system in which water is removed from the tubular lumen and reabsorbed into the circulation. The driving force for reabsorption is the osmotic gradient in the renal medulla which is dependent, in part, on chloride (followed by sodium) pumping from the thick ascending loop of Henle. Urea trapping is also thought to play an important role in the generation of a hypertonic medullary interstitium. Arginine vasopressin (AVP) acts by binding to receptors on the cell membrane and activating adenylate cyclase. This, inturn, results in the intracellular accumulation of cyclic adenosine monophosphate (AMP) which in some fashion abruptly increases the water permeability of the luminal membrane of cells in the collecting duct. As a consequence, water flows along an osmotic gradient out of the tubular lumen into the medullary interstitium. Diabetes insipidus is the clinical condition associated with either a deficiency of or a resistance to AVP. Central diabetes insipidus is due to diminished release of AVP following damage to either the neurosecretory nuclei or the pituitary stalk. Possible causes include idiopathic, familial, trauma, tumor, infection or vascular lesions. Patients present with polyuria, usually beginning over a period of a few days. The diagnosis is made by showing that urinary concentration is impaired after water restriction but that there is a good response to exogenous vasopressin therapy. Nephrogenic diabetes insipidus can be identified by a patient's lack of response to AVP. Nephrogenic diabetes insipidus is caused by a familial defect, although milder forms can be acquired as a result of various forms of renal disease. Central diabetes insipidus is eminently responsive to replacement therapy, particularly with dDAVP, a long lasting analogue of AVP. Nephrogenic diabetes insipidus is best treated with a combination of thiazide diuretics as well as a diet low in sodium and protein.
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PMID:The clinical physiology of water metabolism. Part II: Renal mechanisms for urinary concentration; diabetes insipidus. 54 67

Adrenalectomized rats, kept on tap water for 3 days and infused with the glucocorticoid dexamethasone during the experiment, were compared to similarly treated sham-operated rats. Using the microcatheterization technique, reabsorption of fluid, sodium and potassium in the medullary collecting duct was studied before and after infusion of donor blood (2.3% of body weight). Before intravascular volume expansion sodium excretion in adrenalectomized rats was greater than in sham-operated ones. Extensive overlap between the two groups made this difference not statistically significant. However, the fraction of filtered sodium excreted was significantly greater after adrenalectomy, indicating the expected tubular transport defect. Fluid reabsorption from the medullary collecting-duct system was comparable in both series. Adrenalectomy did not inhibit net sodium reabsorption from the inner medullary duct, although reduction of Na transport in the outer medullary collecting system could be inferred. Renal excretion of potassium was not associated with net K secretion in the collecting duct in either group. During hypervolemia induced by intravenous infusion of donor blood, marked diuresis, natriuresis and kaliuresis were observed in all animals, associated with inhibition of net fluid and sodium reabsorption along the collecting system in both inner and outer medulla. Small, but statistically significant secretion of potassium became evident. The relatively reduced renal response in adrenalectomized animals could be attributed in part to a decreased filtered load compared to sham-operated rats. It is concluded: (1) that lack of mineralocorticoid does not prevent the normal fluid and sodium reabsorption from the lumen of the inner medullary collecting system, and (2) that the inhibition of this reabsorption consequent to hypervolemia is independent of changes in plasma aldosterone levels.
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PMID:Effect of adrenalectomy on medullary collecting-duct function in rats before and during blood volume expansion. 55 99


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