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)

Pregnancy in the rat is accompanied by enhanced reabsorption of salt and water throughout most, if not all, of the gestational period. Many mechanisms have been suggested but definitive answers are still awaited. The major area of controversy centres around the detection of changes at term. There is general agreement that, at least in mid-gestation, the increase in reabsorption can be attributed to increases in the proximal tubules, the loop of Henle and collecting duct. The contribution of the proximal tubule to the increased reabsorption at term is still uncertain. Enhanced salt and water reabsorption is demonstrated in distal nephron segments irrespective of the stage of gestation. Micropuncture and microperfusion experiments have identified increased reabsorption of water, sodium and chloride in the loop of Henle, but it appears that there is net addition of glucose, urea and potassium to the tubular fluid in this segment which, at least for potassium and glucose, offsets to some extent increased reabsorption by the proximal tubule. Altered renal handling of other solutes (uric acid, calcium and magnesium) also occurs throughout pregnancy but the mechanisms responsible and nephron sites involved remain to be investigated. Attempts to attribute altered reabsorption to direct renal effects of changes in maternal hormones are inconclusive. Prolactin mimics some of the pregnancy-associated increases in reabsorption following chronic administration to male and non-pregnant female rats. These effects might be due to a direct renal action of the hormone or even to the volume expansion following its dipsogenic action.
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PMID:Renal tubular function in the gravid rat. 333 Apr 87

Inner medullary collecting duct function in ischemic acute renal failure: The purpose of this study was to determine the role of the medullary collecting duct in the increased urine sodium concentration, decreased urine osmolality, and altered potassium excretion with hyperkalemia which are characteristic of ischemic acute renal failure. Microcatheterization of the inner medullary collecting duct (0.1 to 5 mm from papillary tip) was carried out in rats 24 h after bilateral renal artery clamping for 45 min (n = 8) or sham-operated (n = 8). In ischemic acute renal failure (ARF), tubular fluid osmolality did not increase significantly along the inner medullary collecting duct (IMCD). Tubular fluid sodium concentration was similar to controls at the beginning of the IMCD but was significantly higher at the papillary tip. Tubular fluid to plasma potassium concentration ratio (TF/PK) increased to a greater extent along the IMCD in ischemic ARF than in controls. During acute KCl loading in two additional groups, tubular fluid potassium concentration and TF/PK were much lower at the beginning of the IMCD in ischemic ARF than in controls but increased similarly along the IMCD. In ischemic ARF, with or without KCl loading, renal tissue electrolytes showed reduced potassium concentration in the outer medullary region. The results indicate that impaired IMCD function contributes significantly to the increase in urine sodium concentration and the decrease in urine osmolality which are characteristic of ischemic acute renal failure. In ischemic ARF with mild hyperkalemia, an adaptive increase in K secretion occurred in the IMCD. Severe hyperkalemia and decreased potassium excretion during acute potassium loading in ischemic ARF were determined in more proximal nephron segments and were associated with decreased outer medullary tissue potassium, presumably due to tubular necrosis. Decreased outer medullary tissue potassium could contribute to hyperkalemia by diminishing K secretion in the pars rectae and descending limbs or in the cortical and outer medullary collecting ducts.
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PMID:Inner medullary collecting duct function in ischemic acute renal failure. 340 4

It has been hypothesized that urea from the final urine is recycled into the renal papilla through the pelvic epithelium. To test this hypothesis, samples of urine were collected by micropuncture proximally and distally through the intact, contracting ureter of the anesthetized rat. In 12 rats, in which urine flow was 5.89 +/- 0.67 microliter/min (a moderate antidiuresis), the ratio of proximal-to-distal urea concentration, corrected for water movement, was 0.93 +/- 0.03 (P less than 0.01 compared with unity), indicating that approximately 7% of urea in the urine emerging from the terminal collecting duct was reabsorbed by the time it reached the distal ureter. To assess the possible contribution of urea reabsorption by the ureter, the ureter was cannulated proximally and distally and perfused with urine of known composition at 6.26 +/- 0.10 microliter/min. In nine rats, the ratio of urea concentration in the perfusate collected from the distal end of the ureter to that in the perfusate entering the proximal end was 0.93 +/- 0.02 (P less than 0.01 compared with unity), indicating 7% reabsorption. Movement of solute across the ureteral epithelium was not restricted to urea. Potassium and creatinine were also reabsorbed [3.4 +/- 0.9 (P less than 0.01) and 3.5 +/- 1.2% (P less than 0.05), respectively], whereas sodium was secreted [9.2 +/- 2.3% (P less than 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urea flux in the ureter. 340 82

1. In order to explain the vulnerability of medullary thick ascending limb of Henle's loop (mTAL) during hypoxia, adenosine 5'-triphosphate (ATP) content was measured in isolated rat mTAL cells during control conditions and chemically induced hypoxia and compared with those in medullary collecting duct (MCD) cells. 2. Basal ATP levels in mTAL and MCD were estimated as 3.6 and 2.1 mmol/l, respectively. Antimycin A (5 mumol/l) decreased the ATP content by 41% of the control value in the mTAL cells, but failed to reduce that of the MCD cells. Administration of sodium cyanide (5 mmol/l) drastically depleted ATP in the mTAL cells within 5 min (2-3% of control). On the other hand, ATP levels in MCD cells were sustained for at least 60 min after cyanide administration (64% of control). 3. When tubules were made permeable to sodium by the addition of nystatin, the effects of chemical hypoxia on the cell ATP levels were intensified in both segments, and this was partially blocked by pretreatment with ouabain, or by lowering the sodium concentration of the medium. 4. Higher doses of nystatin in mTAL caused a reduction in ATP levels even under control conditions, but its effect was prevented in low sodium medium. 5. The present study suggests that cell ATP levels can be altered by sodium, potassium-dependent adenosine triphosphatase activity, and that due to their high sodium-transporting activity, mTAL cells are more sensitive to reductions in ATP levels during hypoxia than are MCD cells.
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PMID:A bioenergetic explanation for the selective vulnerability of renal medullary tubules to hypoxia. 341 64

The distal tubule, which includes the thick ascending limb (TAL), the macula densa, and the distal convoluted tubule (DCT), and the collecting duct are structurally heterogeneous, thus reflecting the functional heterogeneity that is also present. As the TAL ascends from medulla to cortex, the surface area of the apical plasma membrane increases while that of the basolateral membrane decreases. The structure of the DCT resembles that of the medullary TAL. An excellent correlation exists between structure, Na-K-ATPase activity, and NaCl reabsorptive capacity in the distal tubule. The collecting duct is subdivided into the initial collecting tubule (ICT), and cortical (CCD), outer medullary (OMCD), and inner medullary (IMCD) collecting ducts. Between the distal tubule and the collecting duct is a transition region termed the connecting segment or connecting tubule (CNT). Considerable structural heterogeneity exists along the collecting duct within the two major cell populations, the intercalated cells and the principal cells. In the CNT, the ICT, and the CCD, potassium loading and mineralocorticoids stimulate Na-K-ATPase activity and cause proliferation of the basolateral membrane of CNT cells and principal cells, thus identifying the cells responsible for mineralocorticoid-stimulated potassium secretion in these regions. Finally, at least two morphologically distinct populations of intercalated cells exist, types A and B. In the rat, type A predominates in the CNT and the OMCD and is believed to be responsible for H+ secretion, at least in the OMCD. Type B predominates in the CCD, where it may be involved in bicarbonate secretion.
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PMID:Structural-functional relationships along the distal nephron. 351 May 62

The distal tubule, which includes the thick ascending limb (TAL), the macula densa, and the distal convoluted tubule (DCT), and the collecting duct are structurally heterogeneous, thus reflecting the functional heterogeneity that is also present. As the TAL ascends from medulla to cortex, the surface area of the apical plasma membrane increases while that of the basolateral membrane decreases. The structure of the DCT resembles that of the medullary TAL. An excellent correlation exists between structure, Na-K-ATPase activity, and NaCl reabsorptive capacity in the distal tubule. The collecting duct is subdivided into the initial collecting tubule (IC), and cortical (CCD), outer medullary (OMCD), and inner medullary (IMCD) collecting ducts. Between the distal tubule and the collecting duct is a transition region termed the connecting segment or connecting tubule (CNT). Considerable structural heterogeneity exists along the collecting duct within the two major cell populations, the intercalated cells and the principal cells. In the CNT, the ICT, and the CCD, potassium loading and mineralocorticoids stimulate Na-K-ATPase activity and cause proliferation of the basolateral membrane of CNT cells and principal cells, thus identifying the cells responsible for mineralocorticoid-stimulated potassium secretion in these regions. Finally, at least two morphologically distinct populations of intercalated cells exist, types A and B. In the rat, type A predominates in the CNT and the OMCD and is believed to be responsible for H+ secretion, at least in the OMCD. Type B predominates in the CCD, where it may be involved in bicarbonate secretion.
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PMID:Structural-functional relationship along the distal nephron. 352 38

The microcatheterization technique was used to examine electrolyte transport in the medullary collecting duct of two groups of anesthetized rats during water diuresis and during a second experimental phase with 1-desamino-8-D-arginine vasopressin (dDAVP) administration or continued water diuresis. Potassium reabsorption of 53-61% of the delivered load was consistently observed in the medullary collecting duct during water diuresis. During dDAVP administration, urinary potassium excretion doubled, and there was no net potassium transport (reabsorption or secretion) in the medullary collecting duct. The change in potassium transport in medullary collecting duct from water diuresis to antidiuresis (dDAVP) was sufficient to account for the increase in urinary potassium excretion. Changes in flow rate, luminal sodium concentration, or collecting duct sodium reabsorption could not account for the changes in potassium transport in the collecting duct during dDAVP. The results are interpreted as indicating that dDAVP stimulates potassium entry (secretion) into the medullary collecting duct, probably by a direct effect. This action of antidiuretic hormone appears to be important in maintaining potassium homeostasis during changing water balance.
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PMID:Effect of vasopressin analogue (dDAVP) on potassium transport in medullary collecting duct. 359 61

The in vivo microcatheterization technique was used to study amiloride-induced transport alterations in the inner medullary collecting duct. Amiloride treated rats (0.1 mg/hr) had significant diuresis and natriuresis, as well as antikaliuresis, compared to untreated controls. The relative decrease in potassium excretion was associated with a significant rise in plasma potassium concentration. Net sodium transport in the duct was decreased from 83 + 3 to 46 + 6 per cent of delivered load, as a result of amiloride treatment. Smaller, but statistically significant, reductions (P less than 0.01) were seen for fluid and chloride reabsorptions (from 66 + 3 to 51 + 4%, and from 72 + 4 to 52 + 5%, respectively). Potassium reabsorption increased from 15 + 8 to 61 + 6% of delivered load. The data indicated that amiloride natriuresis is determined primarily by inhibition of sodium reabsorption in the medullary collecting duct, probably due to blockade of a specific Na channel. The antikaliuresis, on the other hand, appears to be due to inhibition of secretion both in upstream nephron segments and in the duct itself.
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PMID:Effects of amiloride in the medullary collecting duct of rat kidney. 359 52

To investigate the sites of action of aldosterone (Aldo) and chronic potassium loading (high K) and to determine whether dietary K can modulate collecting duct structure independent of Aldo, a morphometric study of the structure of the initial collecting tubule (ICT), the cortical collecting tubule (CCT), the medullary collecting duct in the outer stripe (MCDOS) and the inner stripe (MCDIS), and the papillary collecting duct (PCD) was carried out in a rat model in which plasma levels of Aldo were clamped at basal or physiologically elevated levels and high K could be induced without concomitant hyperaldosteronism. Elevated levels of Aldo increased cell area (Ac) and basolateral membrane surface (BLM) from control values in the ICT, CCT, and MCDOS but not in the MCDIS or PCD. High K with normal physiological levels of Aldo increased BLM in the ICT and CCT without a concomitant change in AC. No response was seen in MCDOS, MCDIS, or PCD. It is concluded that Aldo can modulate principal cell structure in the collecting duct system in segments extending from the ICT through the MCDOS in the rat and that high K independent of Aldo can influence collecting duct structure only in the ICT and CCT.
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PMID:Response of collecting tubule cells to aldosterone and potassium loading. 360 52

Acetazolamide, furosemide, chlorothiazide and amiloride are pharmacologic agents that act primarily in the proximal tubule, loop of Henle, early distal tubule and late distal tubule and collecting duct, respectively. These diuretic agents were used to evaluate the functional integrity of discrete segments of the nephron in the neonatal rat following treatment with a known nephrotoxicant. Six-day old rats were treated s.c. with the proximal tubule toxicant mercuric chloride (1 or 3.2 mg/kg) or saline. Twenty-four hours later, when evidence of mercury nephrotoxicity is detectable, creatinine clearance and the fractional excretion of water and various components of the filtrate were determined using a 2-hr clearance period immediately after injection of a diuretic. The effects of mercury (3.2 mg/kg) were consistent with its ability to cause acute renal failure and proximal tubular necrosis and also indicated an apparent disruption of the cycling of urea in the nephron. A decrease in the fractional excretion of water, combined sodium and potassium and total osmotic solutes indicated that the diuretic response to acetazolamide was markedly attenuated in the mercuric chloride-treated pups whereas the responses to furosemide, chlorothiazide and amiloride were not altered by mercury treatment. Results from this study illustrate the specificity of these diuretics as pharmacologic probes of mercuric chloride induced renal dysfunction and, therefore, support their usefulness as tools in the investigation of renal developmental toxicity.
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PMID:Pharmacologic probing of mercuric chloride-induced renal dysfunction in the neonatal rat. 361 27


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