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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 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

Analysis of the driving forces acting on the movement of potassium across individual membranes of tubule cells shows that both active and passive components play an important role in the regulation of potassium transport. Distal and cortical collecting tubule and papillary collecting duct elements are the key nephron sites participating in a complex fashion to translate a wide variety of metabolic challenges into the appropriate excretory response. The latter involves both secretory and reabsorptive activity. The analysis of the factors modulating tubular potassium transfer has shown that the potassium concentration in the cells of the distal nephron is a dey factactors involved in setting the cellular potassium concentration are active potassium uptake at the peritubular and luminal membrane of the cells as well as electrogenic solium extrusion across the peritubular boundary of the cells. Additional factors regulating potassium transport involve the electrical potential difference, sensitive to changes in the sodium concentration in the lumen, the flow rate past the late distal tubular site of potassium secretion, and the activity of a reabsorptive potassium pump in the luminal membranes of the cells. In the cortical collecting tubule, active potassium secretion is also present at the luminal membrane of the cell, but the role of such an additional secretory mechanism in the late distal tubule is presently unknown. Most of these individual transport mechanisms exist along the whole distal nephron, but their relative prominence varies among the late distal tubule, the cortical collecting tubule, and the papilary collecting duct.
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PMID:Some reflections on the mechanism of renal tubular potassium transport. 120 61

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

To evaluate the effect of hypermagnesemia on distal nephron sodium reabsorption, renal clearance, micropuncture, microinjection, and electrophysiological studies were performed in the anesthetized rat before and after intravenous administration of MgCl2, MgSO4, and Na2SO4. Along the proximal tubule, MgCl2 caused a 21% decrease and MgSO4 a 17% decrease in fractional sodium reabsorption, while only a 4% decrease was observed with Na2SO4. In the loop segment, the decrease in fractional sodium reabsorption was 7% with MgCl2, 15% with MgSO4, and 12% with Na2SO4. In the distal tubule and collecting duct, MgCl2 and MgSO4 had no effect on fractional sodium reabsorption, whereas Na2SO4 significntaly depressed sodium reabsorption to a greater extent in the collecting duct than in the distal tubule. Microinjection studies, however, showed that both MgSO4 and Na2SO4 depressed lumen-to-plasma sodium movement across the collecting duct. Early and late distal tubular transepithelial potential difference was unaffected by MgCl2, whereas it was increased by both MgSO4 and Na2SO4. The decrease in sodium reabsorption along the distal tubule and collecting duct produced by Na2SO4 and probably MgSO4 may relate to the increased transepithelial electrochemical gradient for sodium transport produced by the poorly reabsorbable sulfate anion.
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PMID:Effect of magnesium on rat nephron sodium reabsorption: a segmental analysis. 125 20

Diuretics act primarily by blocking reabsorption of sodium at four major sites in the nephron. Clinically useful agents that block sodium reabsorption effectively in the proximal tubule are lacking. Furosemide (Lasix), ethacrynic acid (Edecrin), and possibly organomercurial agents are effective in the ascending limb of Henle's loop. Thiazides are the major agents acting in the early distal tubule. In the late distal tubule and collecting duct, spironolactone (Aldactone) and triamterene (Dyrenium) are useful, especially in combination with diuretics which act more proximally. In treating edematous states, initial therapy with thiazides is effective in most patients who do not exhibit moderate or severe renal insufficiency, severe hyperaldosteronism with excessive distal reabsorption of sodium in exchange for potassium, or excessive sodium reabsorption in the proximal tubule or ascending limb. Nonedematous states in which diuretic therapy is useful include hypertension, hypercalcemia, hypercalciuria, diabetes insipidus, and acute renal failure.
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PMID:Diuretic agents. Mechanisms of action and clinical uses. 126 95

The present study was undertaken to determine whether the change in cellular Na+ concentration ( [Na+]i) or cellular pH (pHi) is essential for the modulation by Na+/H+ antiporter of the cellular action of arginine vasopressin (AVP) in renal inner medullary collecting duct cells in culture. Extracellular Na+ depletion promptly decreased [Na+]i from 15.8 to 5.4 mM (P less than 0.01), which was closely related to the decrease in pHi (7.19 to 6.97; P less than 0.01). In the presence of 0.5 mM 3-isobutyl-1-methylxanthine, AVP increased cellular cAMP production in a dose-dependent manner. This was significantly blunted in the Na(+)-depleted cells (1 nM AVP; 481.9 vs. 341.0 fmol/micrograms protein; P less than 0.01). When cells were incubated with the Na(+)-depleted medium containing 25 mM NaHCO3, [Na+]i decreased promptly, but the pHi remained unchanged. Under this condition, the AVP-induced increase in cellular cAMP production was not altered (1 nM AVP; 390.9 vs. 334.8 fmol/micrograms protein). Also, after the Na(+)-depleted cells were incubated in 20 mM NH4Cl, which promptly normalized pHi despite the decreased [Na+]i, the response of cAMP production to AVP was restored. Amiloride (1 x 10(-5)-1 x 10(-3) M), which blocks the Na+/H+ exchange, decreased pHi and AVP- and forskolin-induced cAMP production in a dose-dependent manner. These results indicate that the decrease in [Na+]i promptly inhibits AVP-induced cAMP production mediated through the reduction in pHi in renal inner medullary collecting duct cells.
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PMID:pH dependence of inhibition of arginine vasopressin-induced adenosine 3',5'-monophosphate production by cellular sodium depletion in rat renal inner medullary collecting duct cells in culture. 130 26

We studied the cellular pathways of K+ transport by the rabbit cortical collecting duct that was stimulated to absorb Na+ and to secrete K+. The vast majority of K+ secretion (into the lumen) was inhibited by benzamil, a blocker of epithelial Na+ channels. The residual K+ secretion was completely inhibited by ouabain. Thus all active K+ secretion was dependent on Na+ transport by the Na(+)-K+ pump. The passive pathways of K+ transport were further examined using tracer and electrophysiological measurements. K+ transfer across the apical membrane was predominantly or exclusively conductive; the apical K+ conductance was 31 mS/cm2. The basolateral membrane contained two pathways for K+ tracer translocation. The (barium-sensitive) conductive pathway accounted for a relatively small (12-20%) portion of the tracer permeation. A larger pathway appeared to be via K(+)-K+ exchange on the Na(+)-K+ pump. The magnitude of the Ba2(+)-sensitive (basolateral) K+ conductance predicted a substantially larger tracer flux than was actually measured. The best explanation for this difference is the presence of single-file diffusion through K+ channels on the apical and basolateral membranes. An analysis of the electrically silent K+ transport from lumen to bath suggests that the Na(+)-K+ pump can vary the ratio of its Na(+)-K+ and K(+)-K+ modes of operation. When the tubule is actively transporting Na+ and K+, the Na(+)-K+/K(+)-K+ turnover ratio is greater than 7. When Na+ transport is limited by inhibiting Na+ entry across the apical membrane, the ratio falls to less than 1. A major factor determining this ratio is probably the availability of Na+ to the cytoplasmic side of the pump.
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PMID:Analysis of K+ transport by rabbit CCD: conductive pathways and K(+)-K+ exchange by Na(+)-K+ pump. 131 Feb 30


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