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)

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

Prostaglandins have been postulated to participate in the regulation of salt excretion during acute volume expansion. The present papillary and cortical micropuncture studies were designed to examine the effect of prostaglandin synthesis inhibitors on segmental chloride transport during hydropenia (with and without meclofenamate) and 10% volume expansion (with and without both meclofenamate and indomethacin). Both inhibitors significantly decreased the urinary excretion rate of prostaglandins E(2) and F(2alpha). Clearance studies on the intact right kidney demonstrated no effect of either agent on glomerular filtration rate, but a significant reduction in chloride excretion during hydropenia and volume expansion was observed. To assess the specific site(s) of enhanced chloride reabsorption, absolute and fractional chloride delivery was measured in the late proximal tubule, thin descending limb of Henle, and the early and late distal tubules. In addition, the fraction of filtered chloride remaining at the base and tip of the papillary collecting duct was compared to that fraction remaining at the superficial late distal tubule. During hydropenia, meclofenamate had no effect on fractional chloride delivery out of the superficial late distal tubule or the juxtamedullary thin descending limb of Henle, but significantly reduced the fraction of chloride delivered to the base of the papillary collecting duct. During volume expansion, neither meclofenamate nor indomethacin had an effect on absolute chloride delivery out of the proximal tubule or the thin descending limb of Henle. However, absolute chloride delivery to the early distal tubule was significantly reduced, and was associated with a decrease in fractional chloride reabsorption in this segment. Furthermore, the fraction of chloride delivered to the base of the collecting duct was significantly reduced. Fractional reabsorption along the terminal 1 mm of the collecting duct was not altered by either meclofenamate or indomethacin. These results suggest that inhibitors of prostaglandin synthesis result in an increase in chloride reabsorption in the superficial loop of Henle, and in segments between the superficial late distal tubule and the base of the collecting duct. The results are consistent with the view that prostaglandins inhibit chloride transport in the thick ascending limb of Henle, and/or the cortical and outer medullary collecting tubule.
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PMID:Cortical and papillary micropuncture examination of chloride transport in segments of the rat kidney during inhibition of prostaglandin production. Possible role for prostaglandins in the chloruresis of acute volume expansion. 50 Aug 11

After a short review of the functional anatomy of the kidney, we express the usual hypotheses about the phenomena of reabsorption and filtration in the loop of Henle and the collecting duct. Starting from these hypotheses and the laws of biophysics, we formulate the equations of the model. This model accounts for the great increase in concentration of electrolyte and urea in the loop of Henle, the collecting duct and the interstitium, as we "go down" from the outer medullary area towards the inner areas, the active transportation of sodium in the loop of Henle being limited to the thick ascending limb.
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PMID:[Model of the function of the nephron]. 51 80

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

In the anaethetised cat the electrical potential difference between the lumen of the main collecting duct of the pancreas and blood in the jugular vein was measured. The duct was perfused with isotonic solutions of monovalent ions and the recorded potential corrected for the liquid junction potentials. The data were fitted to the Shinagawa extension of the Goldman constant field equation and the relative permeabilities of the duct epithelium to the ions were determined. The duct showed negligible selectivity between the monovalent cations Li:Na:K:Rb:Cs = 1.08:1.10:1.09:1.12 in contrast to the definite selectivity sequence for the anions F:Br:Cl:I:HCO3 = 0.44:1.38:1.08:2.05:0.60. This halide selectivity sequence is the Eisenman sequence I and is indicative of the selectivity being due to weak positive charges on membrane bound sites surrounding a highly hydrated channel. It is argued that these highly hydrated channels may be identified with the "tight junctions" between cells and the selectivity properties of the pancreatic duct are determined by flow of ions through these areas rather than flow through the epithelial cells.
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PMID:The selective permeability of the pancreatic duct of the cat to monovalent ions. 55 48

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

Superficial proximal and distal tubules of both kidneys of pentobarbital-anesthetized cats, infused with 2.5% (w/v) polyfructosan in Ringer solution at 0.45 ml/min, were micropunctured. Whole one-kidney GFR average 4.1 ml/min. SNGFR averaged 15 nl/min in 51 determinations and was proportional to whole-kidney GFR in individual cats. Absolute fluid reabsorption along the length of the accessible portion of the proximal tubule was 1.6 nl/min.mm. The length of the whole proximal tubule was 6 mm as measured from the glomerulum to the descending thin limb of Henle's loop. The length of the distal tubule was 3.5 mm from the macula densa to the first branching of the collecting duct. Proximal fluid was isoosmolar with plasma whereas fluid entering the distal tubule was markedly hyposmolar. Late distal tubular fluid samples were also isosmolar. The cat appears to be well suited for micropuncture experiments in terms of freedom from respiratory movements and the presence of surface distal tubules.
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PMID:Micropuncture study of fluid handling in the cat kidney. 56 46

In a recent study it was found that in Mg loaded rats, the fraction of filtered Mg (% E Mg) recovered in the bend of the loop of Henle of papilla was greater than the filtered load. However, the site of this Mg addition was unspecified and could be either the juxtamedullary proximal tubule, the pars recta, or in the papilla, the descending limb of the loop of Henle. In order to investigate the movement of Mg in the various structures of the papilla, we have studied: 1. The transport of this electrolyte along the collecting duct. 2. Its relative concentration in the loop of Henle and in the adjacent vasa recta. The experiments have been performed in hydropenic and Mg loaded rats. In the collecting duct, the inulin and Mg concentrations increase proportionally, indicating an absence of any transport of Mg along this part of this nephron. In the vasa recta of the accessible papilla, the capillary over peripheral plasma Mg ratio (C/UF Mg) in hydropenia and after Mg loading [1.88 +/- 0.15 (ES) and 2.89 +/- 0.25] were significantly lower than the corresponding TF/UF Mg in the adjacent loops of Henle (2.90 +/- 0.17 and 4.04 +/- 0.37). This finding reduces the possibilities of a Mg passive diffusion from the capillaries to the tubular lumen, unless the electrical potential of the descending limb is more negative than -5 mV. The hypothesis of an active secretion, or a passive diffusion of Mg in the deep proximal tubule, in the pars recta, or in the early non accessible descending limb constitutes the other alternative.
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PMID:Magnesium handling by the papilla of the young rat. 56 20


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