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

The functions of a kidney, whether normal or cystic, can be conceptualized in terms of anatomy (glomerulus, proximal tubule, loop of Henle, distal convolution, and collecting duct), activity (volume regulation, dilution and concentration, acid-base regulation, potassium excretion, transport of organic molecules, and calcium and phosphate excretion), and the integration of anatomic organization to meet functional demand. Our discussion of renal cystic disorders follows this conceptual outline. For discussions of normal renal physiology, the reader is referred to any one of several recent, excellent reviews (1-3). Systematic evaluation of renal function in cystic diseases of the kidney (medullary sponge kidney, medullary cystic disease, and polycystic kidney disease) has only rarely been performed. The available information suggests that the earliest detectable lesions consist primarily of tubular dysfunction. With time, however, significant reduction of glomerular filtration occurs and the resultant accumulation of uremic toxins dominates the clinical picture in polycystic and medullary cystic disease. Significant changes in glomerular function are unusual in medullary sponge kidney. This review represents an attempt to summarize the large body of literature that has accumulated on functional abnormalities in these disorders, and to point out those areas where further investigations are needed.
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PMID:Functional abnormalities in renal cystic diseases. 0 65

This study was designed to determine the effect of acute hyperventilation on distal nephron hydrogen ion secretion. The blood PCO2 declined and stabilized rapidly when bicarbonate loaded rats were hyperventilated. In contrast, the urine PCO2 declined slowly, resulting in an early increase in the urine minus blood (U-B) PCO2 which could not be obliterated by carbonic anhydrase infusion. Within approximately 50 min, the U-B PCO2 in the hyperventilated and carbonic anhydrase infused rats approached zero. Consequently, equilibrium between collecting duct urine and arterial blood PCO2 was then presumed to exist. This provided the basis for the subsequent studies on a series of rats. The U-B PCO2 decreased from a control of 22+/-1 mm Hg (mean+/-SEM) to 11+/-2 mm Hg (mean+/-SEM) with hypocapnia, and rose again to its control value when the blood PCO2 returned to prehyperventilation values. This decline in U-B PCO2 with acute hyperventilation could not be attributed to changes in urine flow, phosphate, or bicarbonate excretion, suggesting, therefore, a decrease in distal nephron (probably collecting duct) hydrogen ion secretion with acute hyperventilation. Possible pitfalls in the interpretation of the UB PCO2 are illustrated.
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PMID:The effect of hyperventilation on distal nephron hydrogen ion secretion. 0 92

1. The proposition that changes in renal calcium excretion during vasopressin administration are positively correlated with concurrent changes in urine hydrogen ion concentration was tested by administration of vasopressin into twelve conscious diuresing sheep receiving either alkalinizing or acidifying infusions. 2. Vasopressin-induced antidiuresis in sheep with alkaline urine was associated with significant increases in urinary pH and decreases in the rate of calcium excretion whereas antidiuresis in sheep with acid urine was associated with significant decreases in urinary pH and no consistent effect on calcium excretion. 3. Magnesium excretion increased during vasopressin administration in most experiments regardless of urinary pH changes. 4. Vasopressin administration did not significantly alter the rate of excretion of sodium, potassium, chloride and phosphate or the rates of sodium, potassium, chloride, inulin, para-aminohippurate and osmolal clearance in sheep with either acid or alkaline urine. Potassium excretion and clearance in sheep with alkaline ruine was higher than that of sheep with acid urine during vasopressin infusion. 5. The results support the hypothesis that changes in renal tubular hydrogen ion concentration or bicarbonate concentration caused by water reabsorption from the collecting duct and possibly the late distal tubule could be part of the explanation for changes in renal calcium excretion which occur during vasopressin-induced antidiuresis.
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PMID:Renal calcium and magnesium excretion during vasopressin administration into sheep with acid or alkaline urine. 4 39

The question of phosphate transport along the collecting duct remains controversial inasmuch as no data from direct in vivo evaluation of this nephron segment have been reported. We measured net phosphate transport along the inner medullary collecting duct (IMCD) using the collecting duct microcatheterization technique in five groups of rats. In control rats no net phosphate transport was found and 9.4% of the fraction of filtered phosphate (FFP) entered the IMCD and was excreted. After acute thyroparathyroidectomy (TPTX) there was a striking reduction in the FFP entering the IMCD, 1.8%, and significant reabsorption occurred, 0.5% being excreted. With acute TPTX and parathormone infusion, delivery increased to 33% without significant change along the IMCD. With acute TPTX and phosphate infusion, delivery was increased to control levels but no change was found in net phosphate transport. In rats studied 5-7 days after uninephrectomy alone, phosphate delivery was greater than in control, 25%, and no net phosphate transport was found. These studies demonstrate that phosphate absorption occurs along the IMCD in acutely TPTX rats when the delivery of phosphate to the IMCD is markedly reduced. The increase in phosphaturia which occurs after a reduction in renal mass cannot be accounted for by changes in net phosphate transport along the IMCD.
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PMID:Phosphate transport along the inner medullary collecting duct of the rat. 46 60

Renal micropuncture and microdissection techniques with ultramicro fluid analysis have been applied to evaluate single nephron function in the skate, Raja erinacea. We have divided the skate nephron into three proximal tubular segments (PTS I-III), three distal coilings (DC I-III), and a countercurrent loop system located between the proximal segments and the distal coilings. The collecting duct is the principal site of urinary dilution. Following exposure of the fish to 75% seawater for about 24 hours, the sodium concentration difference between the end collecting duct lumen and plasma is decreased sufficiently to account for the urinary dilution. The principal site for magnesium, phosphate and sulphate secretion appears to be PTS II. This segment is located on the ventral surface of the kidney. PTS II is also the main nephron site for reabsorption of sodium and chloride in excess of water.
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PMID:Renal tubule ion transport and collecting duct function in the elasmobranch little skate, Raja erinacea. 85 Jan 20

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 mechanism of glomerular dysmorphic cell formation was studied in a in vitro system simulating the process of concentrated acidic urine formation along the nephron. Red cells suspended in phosphate buffer were exposed to three sequential pH gradients, (1) pH 7.4-6.6, (2) pH 6.6-6.5, and (3) pH 6.5-5.2, accompanying osmolality gradients, (1) 280-1200 mOsm/kg H2O, (2) 1,200-140 mOsm/kg H2O, and (3) 140-1,100 mOsm/kg H2O, respectively, for 15 to 60 min, and red cell shapes were observed by differential interference microscopy. The appearance rate of glomerular dysmorphic cells was 37.7 to 47.1% after finishing all the gradients. The last gradient, simulating the work of the collecting duct, was essential for the dysmorphic cell formation; maximal formation was at the final pH of 5.0 and osmolality of 1,000 mOsm/kg H2O. No dysmorphic cells were observed in gradients simulating alkaline or diluted urine formation. In 10 glomerulonephritic patients, glomerular dysmorphic cells appeared over five times as frequently in concentrated acidic urine as in alkaline or diluted urine. Results of in vitro and patient studies coincided well with each other, suggesting that in glomerulonephritic patients, dysmorphic cells might be produced while red cells are passing through the tubules, where concentrated acidic urine is formed.
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PMID:The mechanism of glomerular dysmorphic red cell formation in the kidney. 147 90

Calcium channel blockers have diuretic and natriuretic properties in normal animals and humans. The renal mechanism by which this natriuresis is produced has not yet been completely defined although dihydropyridine derivatives evoke it in experimental animals independently of any effects on renal blood flow or on the glomerular filtration rate. Injections or infusions into the renal artery indicate that the renal excretory effect is secondary to a direct action on renal tubular water and solute reabsorption but not to renal hemodynamic changes. Studies undertaken to localize the site of action of dihydropyridine calcium antagonists on renal tubules by renal clearance and micropuncture techniques suggest that both proximal and distal tubular sites are involved. Primary sites of action in distal convoluted tubules and in the collecting duct have been identified for felodipine and nisoldipine during sodium infusion, whereas sites for nitrendipine in proximal tubules have been demonstrated in strict hydropenia. Both changes in the tubuloglomerular feedback setting and suppression of aldosterone secretion have been proposed to explain some of these effects. The changes do not, however, seem to be dependent on renal innervation. In normal humans, the degree and duration of natriuresis and diuresis correlate with the dose of dihydropyridine derivatives and the extent of systemic pressure reduction. Clearance studies of normal subjects indicate an effect of different dihydropyridine derivatives on tubular fluid and electrolyte reabsorption. Nicardipine and nifedipine are reported to exert proximal tubular actions based either on urate and phosphate excretion or water and lithium clearance. The measurement of tubular indices following felodipine administration suggests a proximal tubular site of action.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal tubular effects of calcium antagonists. 161 68

Phosphate transport by the inner medullary collecting duct of normal rats was studied using an in vitro microperfusion technique. Net (Jnet), lumen-to-bath (Jlb) and bath-to-lumen (Jbl) phosphate fluxes were measured using 32PO4 as tracer, in the absence of net water absorption. A net absorption of phosphate (22.3 +/- 3.3 pmol cm-2 s-1) was observed by direct determination, and was similar to the difference between the Jlb and Jbl (57.7 +/- 8.2 and 32.2 +/- 1.5 pmol cm-2 s-1 respectively). The addition of amiloride (10 microM) to the perfusate did not change the Jlb of phosphate but blocked the efflux of sodium. Also, the withdrawal of sodium from the bath and perfusion solution did not change the Jlb of phosphate. In parallel, the addition of ouabain (10 mM) to the bath fluid decreased the Jlb of sodium more (37%) than the Jlb of phosphate (12%) and did not change the Jbl of phosphate. The addition of arsenate (10 microM) to the perfusate both in the presence and in the absence of sodium caused a decrease in Jlb, but Jbl remained unchanged, and parathyroid hormone (10 U) added to the bath did not change the Jlb. The increase in pH of the bath and perfusion fluid was associated with an increase in the Jlb of phosphate, and the decrease in pH was similarly followed by a decrease in phosphate efflux. The Jbl did not change with the pH alterations. These data demonstrate that a net phosphate absorption takes place in rat inner medullary collecting duct perfused in vitro and that this transport appears to be independent of sodium absorption and the action of parathyroid hormone. Moreover, a decrease in luminal and bath pH induces a decrease in phosphate efflux.
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PMID:Phosphate transport in isolated rat inner medullary collecting duct. 161 29

Na+ entry into kidney epithelial cells occurs by a multiplicity of pathways. Established cell lines such as the A6 cells, derived from the collecting duct of the kidney of Xenopus laevis, MDCK cells, from the distal tubule of a dog kidney, and the LLC-PK1 cells, originating from the proximal tubule of a pig kidney, provide excellent model cell systems for the detailed characterization and isolation of the proteins which comprise these entry pathways. Major pathways of Na+ entry include the amiloride-sensitive Na+ channel, the amiloride-sensitive Na+/H+ antiporter, and the loop diuretic-sensitive NaCl/KCl symporter. While the former two systems have been shown to exhibit an apical location in epithelial cells so far examined, the last system may be localized to either the basolateral or apical surface, depending on the transport function of the cell. Nutrient/Na+ symporters such as the glucose, phosphate, and p-aminohippurate symporters may all be localized to the apical surfaces of proximal tubular cells, but other systems, including those specific for neutral amino acids, may predominate in the basolateral surface or be distributed between the two membranes. Studies concerned with the catalytic, structural, and regulatory properties of these transport systems serve not only to characterize the individual translocators in established cell lines, but also to suggest their physiological functions in intact kidney tissues.
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PMID:Sodium entry pathways in renal epithelial cell lines. 242 Nov 47


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