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

Using a microcatheterization technique, the contribution of the collecting duct to the renal response to extracellular fluid volume expansion was studied in anesthetized rats. During intravenous infusion of Ringer solution (0.25 ml/min per 100 g body wt), urinary excretion of fluid, sodium, and potassium was 365 mul/min per g kidney wt (V), 52.6 mueq/min per g kidney wt (UNaV), and 3.86 mueq/min per g kidney wt (UKV), representing 23, 24, and 65% of filtered load, respectively. Analysis of collecting duct fluid from cortex and outer medulla indicated continued net reabsorption of ions and water in these nephron segments; in contrast, in inner medulla net secretion of Na, K, and fluid into the collecting duct was demonstrated. Addition of sodium and water was equivalent to approximately 10% of filtered load. It is concluded that under the stress of extreme intravenous fluid loading tubular secretion of salt and water into the inner medullary collecting duct contributes importantly to diuresis and natriuresis. The mechanism of such secretion remains undetermined.
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PMID:Secretion of salt and water into the medullary collecting duct of Ringer-infused rats. 111 77

The permeability of the tight junctions (zonulae occludentes) was evaluated along the entire length of the collecting duct of the rat using a lanthanum tracer technique. Nine rats with hereditary hypothalamic diabetes insipidus were studied using standard micropuncture and clearance techniques. Glomerular filtration rate (GFR) estimated from inulin clearance, urine and plasma osmolality (U/Posm) and urine flow rate (V) were determined in eight of nine animals. During either sustained diuresis (five animals) or vasopressin-induced antidiuresis (four animals), individual surface convolutions of distal convoluted tubules or early cortical collecting ducts were preserved for ultrastructural examination by intraluminal microperfusion with a glutaraldehyde-formaldehyde fixative followed by a second microperfusion with a lanthanum tracer. Mean GFR during diuresis was 6.31 plus or minus se 0.63 ml/min/kg of body wt and v=797 plus or minus se 108 mul/min/kg or 13.6 plus or minus se 2.2% of the filtered load of water. After administration of exogenous vasopressin, V fell to 311 plus or minus 157 mul/min/kg or 5.2 plus or minus se 3.8% of the filtered load of water and U/Posm rose from 0.658 plus or minus se 0.043 to 2.124 plus or minus 0.454. Tight junctions of cortical and outer medullary segments of the collecting duct resisted lanthanum penetration. Tight junctions of the inner medullary and papillary segments of the collecting duct were freely permeable to lanthanum suggesting the presence of a paracellular shunt pathway for solute and water movement. The results were independent of the presence or absence of vasopressin. Physiological studies have previously demonstrated that cortical and outer medullary segments of the collecting duct have a low urea permeability while inner medullary and papillary segments of the collecting duct have a relatively high urea permeability. The possibility is suggested that urea movement across the inner medullary and papillary segments of the collecting duct may occur, at least in part, via a paracellular pathway formed by the nonoccluding tight junction and the lateral intercellular space.
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PMID:Lanthanum permeability of tight junctions along the collecting duct of the rat. 112 64

The concentration of major urinary solutes was studied in ureteral urine collected at 15- to 30-s intervals at the onset of acute diuresis induced in anesthetized dogs either by high-ceiling diuretics (mainly ethacrynic acid) or by osmotic diuretics. Phosphate/inulin clearance ratios remained unchanged; potassium/inulin clearance ratios rose rapidly. Principal attention is given to the mechanisms underlying a transient rise in urinary sodium and chloride concentrations during the onset of diuresis. When the data are corrected for washout artifacts from the pelvis and ureter, it can be shown that the initial collection periods are associated with a transient increase in free-water production and by the simultaneous secretion of urea from the interstitium into the tubular fluid. The former coincides in time with the rise in urinary chloride concentration and represents an augmentation of water reabsorbed in the collecting duct, which is relatively impermeable to chloride. Both responses are quantitatively consistent with the transition from a hyperosmotic to isosmotic medullary interstitium.
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PMID:Electrolyte excretion and free-water production during onset of acute diuresis. 113 May 34

The renal handling of urea has been investigated with the aid of a computer model of the countercurrent system in which active electrolyte reabsorption occurs along the entire ascending limb of Henle's loop. In this model, summarized in Fig.9, the buildup of a corticopapillary gradient for urea is optimized if there is net addition of urea to loops of Henle only in the outer medulla. This added urea remains within the tubular system until it is reabsorbed from collecting ducts in the inner medulla. Thus, a net transfer of urea from outer to inner medulla is accomplished (via distal tubule and cortical collecting duct). There is no net addition of urea to loops of Henle within the inner medulla; in this region, the loops act simply as countercurrent exchangers for urea. Computer simulation of systematic variation in the urea permeabilities of each nephron segment shows that interference with any element of the above schema results in impairment of the medullary accumulation of urea relative to plasma. Simulation of varying rates of urinary urea excretion demonstrates that this model can account for the ability of the kidney to excrete substantial amounts of urea without an accompanying osmotic loss of water. The major insight gained from this study is that net addition of urea to loops of Henle in the outer medulla greatly enhances the medullary accumulation of urea, whereas, net addition of urea to loops within the inner medulla tends to defeat such accumulation and hence the urinary concentrating process. This general principle applies also to an alternate model of the countercurrent system, in which electrolyte reabsorption from thin ascending limbs of Henle is passive.
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PMID:Urea handling by the renal countercurrent system: insights from computer simulation. 117 37

Blood-perfused isolated dog kidneys demonstrate steady increases in blood flow and in water and sodium excretion which could be attributed to the accumulation of renal prostaglandins in the perfusing blood. This hypothesis was tested by adding indomethacin, a potent inhibitor of prostaglandins synthesis, to the perfusing blood. Indomethacin completely prevented the vasodilation observed in control kidneys, without affecting glomerular filtration rate. Urine volume was not modified but sodium excretion was enhanced while the steady free water clearance increment observed in the control kidneys was depressed by indomethacin. The sum of sodium and free water clearances which, in the absence of antidiuretic hormone, constitutes an index of the part of the filtered load of solutes which escapes proximal tubular reabsorption, was not modified by indomethacin. Finally, indomethacin partially maintained the osmotic cortico-papillary gradient which was abolished after 2 hrs perfusion in control kidneys. These data suggest that prostaglandins accumulation in the blood is probably the major cause of the vasodilation taking place in isolated blood-perfused kidneys. This vasodilation does not account for decreased proximal reabsorption but partially explains the ADH-resistant diabetes insipidus developing in the isolated kidney. Moreover, indomethacin inhibits sodium reabsorption in the ascending limb of Henle's loop and increases water transport in the collecting duct.
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PMID:Effects of indomethacin on renal hemodynamics and on water and sodium excretion by the isolated dog kidney. 123 89

The distribution of kallikrein in dog kidneys was studied. It was found that kallikrein decreased from the outer to the inner cortex and that the medulla and papilla had very little kallikrein. The site of kallikrein secretion in the nephron was also studied by performing stop-flow techniques in dogs. The highest kallikrein concentration was found in the fractions with the lowest sodium concentration. It was concluded that kallikrein is secreted into the urine at the level of the distal tubule by either the tubule itself or by a structure related to this part of the nephron. In addition, the possible involvement of the kallikrein-kinin system in the regulation of sodium excretion was investigated. Circulating kinins and urinary kallikrein were increased in saline-loaded dogs. Urinary kallikrein also increased in dogs that have "escaped" the sodium-retaining effect of desoxycorticosterone. Experiments in rats with different sodium intake showed a relationship between water and sodium excretion and urinary kallikrein. These data suggest that the kallikrein-kinin system could participate in the regulation of the renal function at the level of the distal tubule or collecting duct.
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PMID:Renal kallikrein: its localization and possible role in renal function. 124 53

Fluid reabsorption in surface nephrons was studied by micropuncture 3 hours after release of complete left ureteral ligation (LUL) or after unilateral release of bilateral ureteral ligation (BUL). In 11 rats with LUL, glomerular filtration rate (GFR) averaged 0.23 +/- 0.04 ml. per minute in the experimental vs. 1.25 +/- 0.11 ml. per minute in the control kidney. GFR averaged 0.18 +/- 0.02 ml. per minute in BUL. Single nephron glomerular filtration rate (SNGFR) was decreased in the experimental kidney of LUL or BUL when determined at proximal or distal sites as compared to the SNGFR determined in shams or the left kidney following right ureteral ligation (RUL). Fractional water excretion was increased after release of obstruction. LUL 2.72 +/- 0.66 per cent; BUL 12.3 +/- 2.82 per cent when compared to sham-operated rats (0.48 +/- 0.07 per cent) or to the untouched kidneys of the RUL group (0.60 +/- 0.09 per cent). Despite increased water and sodium excretion after release of unilateral ureteral ligation and BUL there were marked differences in tubular fluid reabsorption between these two groups. Following release of LUL there was increased fractional water reabsorption along the accessible length of surface nephrons of the experimental kidney. At 55 per cent of proximal tubular length TF/Pin averaged 4.02 +/- 0.02 in LUL vs. 2.18 +/- 0.06 in shams. The mean TF/Pin at 90 per cent of distal tubular length was 31.0 +/- 1.37 in LUL vs. 10.6 +/- 0.08 in sham-operated rats. In contrast, water reabsorption after BUL was slightly but significantly suppressed proximally (TF/Pin 1.95 +/- 0.02) and markedly depressed distally (TF/Pin 3.35 +/- 0.29). These results suggest that the change in fluid reabsorption observed after relief of LUL is located at a site beyond the accessible length of surface nephrons, most likely in the collecting duct. However, the data could also be explained by alterations in fluid reabsorption in deep nephrons. The changes in fluid reabsorption seen following release of BUL reflect the additive effects of release of obstruction and a marked reduction in functioning nephron mass.
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PMID:On the site of decreased fluid reabsorption after release of ureteral obstruction in the rat. 124 72

CHIP28 is an integral membrane protein that has been identified as the erythrocyte water channel and that is also expressed in the kidney. Antibodies against erythrocyte CHIP28 were used to localize this protein along the rat urinary tubule. By Western blotting, CHIP28 was detected in kidney plasma membrane and endosome fractions. With the use of immunocytochemistry, CHIP28 was located in brush-border and basolateral plasma membranes of the proximal tubule. The initial S1 segment was weakly stained, but the S2 and S3 segments were heavily labeled. Subapical vesicles were also positive. Apical and basolateral membranes of the long thin descending limb were strongly labeled, but ascending thin and thick limbs of Henle and distal convoluted tubules were negative. Some vasa recta profiles in the medulla were positive. CHIP28 is, therefore, present in membranes with a high constitutive water permeability, where it probably acts as a transmembrane water-conducting channel. Finally, a weak staining of apical and basolateral membranes of cortical collecting duct principal cells was detectable, suggesting a potential relationship of CHIP28 to the vasopressin-sensitive water channel.
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PMID:Localization of the CHIP28 water channel in rat kidney. 128 99

The influence of avian atrial natriuretic factor (ANF) on renal function was examined in conscious saltwater-acclimated Pekin ducks undergoing a steady state diuresis maintained by iv infused isotonic avian Krebs-Ringer solution at a rate of 1.0 ml/min. Synthetic chicken ANF (chANF) was applied iv at doses of 10, 50, and 90 ng/min.kg BW for 10 min and caused dose-dependent transient increases in urine flow, osmolal excretion, glomerular filtration rate, effective renal plasma flow, and fractional water clearance at decreased urinary osmolality. Using receptor autoradiography, binding sites for [125I]Bolton-Hunter-labeled chANF [( 125I]BH-chANF) were localized in both the reptilian-type glomeruli and the collecting duct system throughout the duck kidney. A RRA for [125I]BH-chANF, established using an enriched kidney membrane fraction, indicated that unlabeled chANF and human ANF competitively displaced [125I]BH-chANF with comparable potencies. ANF-induced modulation of renal salt and water elimination via glomerular and tubular receptor interactions is consistent with the concept that this hormone has a physiological role in avian volume homeostasis.
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PMID:Modulation of kidney function in conscious Pekin ducks by atrial natriuretic factor. 131 Feb 79

Endothelins may be important regulators of renal inner medullary collecting duct (IMCD) function. These peptides are secreted in large amounts by IMCD cells and can, in turn, potently inhibit sodium and water transport systems in the IMCD. This study characterized endothelin (ET) receptors in the IMCD in order to gain insight into this unique renal autocrine system. Radioligand binding studies with 125I-ET-1 yielded a B(max) of 205.7 fmol/mg and a KD of 218 pM for ET-1. Similar studies with 125I-ET-3 yielded two populations of receptors for ET-3, one with a KD of 50 pM and one with a KD of 920 pM. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of IMCD cells covalently labeling with 125I-ET-1 yielded two bands, one at 97 kDa with affinities of ET-1 greater than ET-2 much greater than ET-3 and one at 47 kDa with affinities ET-1 greater than or equal to ET-2 = ET-3. Reverse transcription and polymerase chain reaction revealed the presence of both endothelin receptor types A and B. These data indicate that IMCD cells have high affinity, high density receptors for endothelin and express both known types of endothelin receptor.
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PMID:Characterization of endothelin receptors in the inner medullary collecting duct of the rat. 131 15


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