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)

The mechanism of Ca2+ transport by various segments of the distal nephron was studied in vitro using the isolated perfused tubule technique. Calcium absorption in the distal convoluted tubule (DCT) and the granular portion of the cortical collecting duct (CCTg) was significantly enhanced in the presence of parathyroid hormone (PTH), 3 X 10(-2) U/ml. Na+ was absorbed from and K+ was secreted into the lumen of the DCT. The presence of amiloride (5 X 10(-5) M) or furosemide (5 X 10(-5) M) in the perfusate of DCT each caused a partial inhibition of Na+ but not Ca2+ absorption. The foregoing result with Na+ is consistent with the heterogeneous nature of DCT. Net Na+ absorption and K+ secretion also occurred in the CCTg; both processes were completely inhibited by amiloride. Ca2+ absorption occurred in the thick ascending limb of Henle's loop; it was not enhanced by PTH, and the results were consistent with passive movement. No net Ca2+ movement was observed in the nongranular (light) segment of the cortical collecting tubule in the presence or absence of PTH or dibutyryl cyclic adenosine monophosphate.
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PMID:Calcium transport across segments of the rabbit distal nephron in vitro. 21 62

The concentration of nine endogenous free L-alpha-amino acids (ALA, LEU, ILE, PHE, TYR, LYS, GLU, PRO, GLY) and of taurine were determined simultaneously along the nephron of the rat kidney using free-flow micropuncture techniques without altering plasma amino acid concentration or kidney function. The amount of each amino acid was determined after dansylation (14C-labelled dansyl-chloride) in the micropuncture sample followed by thinlayer chromatography. The main site of reabsorption is the proximal tubule. After 15-20% of the proximal tubule length the bulk of reabsorption has taken place (18.9 plus or minus 3.4% S.E. of the filtered load remaining). Net reabsorption continues to a small but significant extent along the distal nephron (disal tubule and collecting duct). Reabsorption of taurine is less rapid (% remaining of filtered load at the early proximal tubule 37.0 plus or minus 4.6%). The transtubular concentration ratio of all amino acids except taurine follows a homogeneous course. Under the experimental conditions of this study no distction with respect to different systems of reabsorption "neutral", "basic", "acidic", "imino-glycine") could be made.
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PMID:Amino acid reabsorption in the rat nephron. Free flow micropuncture study. 117 57

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

Free-flow micropuncture and in situ microperfusion techniques were used to define the site of action and relative effect of MK447 [2-aminomethyl-4-(1,1-dimethylethyl)-6-iodophenol hydrochloride] vs. furosemide in the rat kidney. MK447 was administered i.v. at 5 mg/kg/hr. Infusion of this drug had little effect on proximal tubule reabsorption of water, Na+ and K+. In contrast, reabsorption of these constituents by the loop of Henle was significantly reduced. There was a tendency for water and Na+ reabsorption to rise and for K+ secretion to fall along the distal tubule. These latter effects can be explained by the contributions of an increased distal flow rate and increased tubule fluid K+ concentration. Net addition of K+ beyond the distal tubule was observed. This may be due to effect of the drug on the collecting duct system or juxtamedullary nephrons. The effects of MK447 and furosemide on loop of Henle reabsorption were compared in microperfusion experiments. Furosemide reduced Na+, K+ and water reabsorption by the loop, whereas MK447 had no effect. A 6-bromophenol sulfate ester of MK447 significantly reduced loop reabsorption. From these observations, we conclude that MK447 affects water and electrolyte reabsorption by the loop of Henle and beyond the superficial late distal tubule. The fact that a potential metabolite, but not MK447, significantly reduced reabsorption by the in situ, perfused loop of Henle supports the hypothesis that the p.o. and i.v. effects of MK447 are dependent on metabolism.
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PMID:Micropuncture evaluation of the site of action of 2-aminomethyl-4-(1,1-dimethylethyl)-6-iodophenol hydrochloride (MK447) in the rat kidney. 199 96

Newborn rabbits maintain a state of hypochloremic metabolic alkalosis with plasma HCO3- concentrations generally exceeding 27 mM. The large amounts of potential net base in mother's milk probably contribute to the generation of this alkalosis. We surmised that immature handling of H+ or HCO3- by the neonatal collecting duct helps maintain this alkalosis. Net HCO3- transport was measured in perfused collecting ducts taken from maturing rabbits, in solutions simulating adult rabbit plasma ultrafiltrate and then in presence of Cl(-)-free bathing solution. Cortical collecting ducts (CCD) from newborn and 4-wk-old rabbits failed to secrete HCO3- under baseline conditions and could not be stimulated to secrete HCO3- in Cl(-)-free bath. Neonatal segments perfused at very slow flow rates showed significant HCO3- absorption; inhibition of HCO3- secretion by removal of luminal Cl- revealed a substantial HCO3- absorptive flux. Segments from 6-wk-old and mature animals secreted net HCO3- and generally showed more than a fivefold increase in HCO3- secretion after Cl- removal from the bath. Outer medullary collecting ducts (OMCD) from newborn rabbits absorbed HCO3- at rates approaching that of mature segments. We conclude that relatively high rates of HCO3- absorption in OMCD and lack of HCO3- secretion in CCD may contribute to the metabolic alkalosis of the neonatal rabbit.
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PMID:Maturation of HCO3- transport in rabbit collecting duct. 224 Feb 33

Ca2+ transport by the inner medullary collecting duct (IMCD) of normal rats was studied using the "in vitro" microperfusion technique. Net (Jnet), lumen-to-bath (Jl----b), and bath-to-lumen (Jb----l) fluxes of Ca2+ were measured in the absence of net water absorption using 45Ca as a tracer. In the absence of an electrochemical gradient, an important net absorption of Ca2+ (11.1 +/- 1.6 pmol.cm-2.s-1), similar to the difference between the Jl----b and Jb----l, was observed by direct determination at low (5-6 nl/min) and high (12-17 nl/min) perfusion rates. The Jl----b of Ca2+ was reduced by the addition to the bath fluid of ouabain (10(-3) M) and verapamil (10(-4) M), by the presence of amiloride (10(-5) and 10(-3) M) and verapamil (10(-4) M) in the luminal fluid, or by perfusion with a Na+-free solution. Neither the presence of verapamil (10(-4) M) and ouabain (10(-3) M) in the bath nor the withdrawal of Na+ from bath and perfusion solution was able to modify the Jb----l of Ca2+. Incrementing Ca2+ bath concentration increased proportionally the Jb----l of Ca2+. Therefore Ca2+ outflux is in part dependent on Na+-K+-adenosinetriphosphatase luminal membrane Na+ transport and in part inhibited by verapamil. However, Ca2+ influx is independent of Na+ transport, is not blocked by verapamil, but is increased by Ca2+ transtubular gradient, indicating the presence of a passive diffusion mechanism.
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PMID:Calcium transport across rat inner medullary collecting duct perfused in vitro. 258 80

Mineralocorticoid plays a role in urinary acidification and acid-base balance, but the response of the inner medulla to aldosterone has not been elucidated. A model of selective aldosterone deficiency (SAD) with hyperkalemia and hyperchloremic metabolic acidosis was employed to assess segmental acidification by measuring in situ pH, titratable acidity (TA) and total ammonia (Am). Hydrogen ion secretion was also examined as a function of the increment in in situ PCO2 in the collecting duct during bicarbonate loading. SAD rats were compared to ADX controls that received adrenalectomy and chronic replacement of gluco- and mineralocorticoid and to rats with chronic metabolic acidosis induced by oral NH4Cl (CMA). Both fractional and absolute delivery of Am to the loop of Henle was lower in SAD vs. CMA rats (1.34 to 3.63 mM, P less than 0.01). Delivery of Am to the base and tip collecting duct (BCD and TCD) was also markedly lower in SAD (1.50 vs. 0.52 and 1.77 vs. 0.47 mM, respectively, P less than 0.01). Net addition of Am and net acid between BCD and TCD, observed in CMA rats, was not observed in SAD despite equivalent degrees of systemic metabolic acidosis. Similarly, the concentration gradient favoring transfer of NH3 between loop of Henle and CD was reduced in SAD. During bicarbonate loading the increment in PCO2 at BCD, TCD and in final urine was significantly lower in SAD rats than in adrenal intact bicarbonate-loaded rats. Therefore, the acidification defect in this model of SAD appears to be a result of a decrease in ammonia production and delivery to the loop of Henle, impaired transfer from loop to collecting duct and reduction in the rate of H+ secretion by the collecting duct.
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PMID:Effect of selective aldosterone deficiency on acidification in nephron segments of the rat inner medulla. 318 58

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

Electrophysiological and chemical methods were used to determine the Na and K transport properties of the isolated cortical collecting duct (CCD) of control and adrenalectomized (ADX) rabbits. Net fluxes of Na (JNa) and K (-JK) in controls were 5.7 and 3.2 pmol . mm-1 . min-1 and in ADX were 1.0 and 0.7 pmol . mm-1 . min-1, respectively, similar to electrically determined rates. In separate experiments, blind impalement of cells from adrenal intact (group 1), ADX (group 2), and ADX rabbits treated with deoxycorticosterone (group 3) allowed identification of two distinct cell types, majority cells (MA) and minority cells (MI). In all groups, MA were distinguished from MI by a relatively high basolateral membrane potential (-Vb), low apical membrane fractional resistance (FRa), and presence of apical and basolateral membrane K conductances. Vb of MA (-82.4 mV) was significantly hyperpolarized in groups 1 and 3 combined, when compared with group 2 (-66.4 mV). However, there was no significant difference between Vb of MI in group 2 (-38.9 mV) and Vb of MI in groups 1 and 3 (-36.2 mV). In MA of group 1 equivalent circuit values of apical membrane Na and K conductances (GNaa, GKa) and maximum pump current (Ipmax) were 0.84 and 6.72 mS/cm2 and 46.7 microA/cm2, respectively. These values in group 2 were significantly lower (0.28 and 1.52 mS/cm2 and 8.7 microA/cm2, respectively). It is concluded that two cell types can be distinguished electrically in the CCD. MA have properties consistent with principal cells and MI have properties consistent with intercalated cells. ADX causes a decrease in GNaa, GKa, and Ipmax of PC that results in proportionate decreases in INaa and IKa.
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PMID:Effects of adrenalectomy on CCD: evidence for differential response of two cell types. 366 23

To assess the role of cortical collecting duct bicarbonate secretion in the regulation of net acid excretion, we have sought to identify what factors influence the secretion rate. Net and unidirectional bicarbonate fluxes were measured in isolated perfused cortical collecting ducts from deoxycorticosterone-treated rabbits. The collecting ducts secreted bicarbonate at 11-24 pmol X mm-1 X min-1, confirming the high rate seen in earlier studies. Oral acid loading (50 mM NH4Cl drinking water) completely inhibited the net bicarbonate secretion. The bath-to-lumen flux was markedly reduced with acid loading, but the lumen-to-bath flux changed very little. In tubules from rabbits treated with deoxycorticosterone (but not NH4Cl), luminal chloride replacement with either sulfate or gluconate completely and reversibly inhibited the net bicarbonate secretion. The bath-to-lumen flux was greatly inhibited, but there was little change in the lumen-to-bath flux. We conclude: 1) High rates of bicarbonate secretion can be induced in rabbit cortical collecting ducts by chronic treatment of the animals with deoxycorticosterone. 2) When deoxycorticosterone-treated rabbits were made acidotic by oral administration of NH4Cl, the bicarbonate secretion was prevented, indicating that the systemic acid-base state of the animal may be an important factor regulating bicarbonate secretion. 3) Replacement of chloride in the lumen with sulfate inhibits bicarbonate secretion in the cortical collecting duct, an effect which may explain in part the decrease in urinary pH in response to sulfate infusions in mineralocorticoid-stimulated animals.
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PMID:Deoxycorticosterone-stimulated bicarbonate secretion in rabbit cortical collecting ducts: effects of luminal chloride removal and in vivo acid loading. 392 46


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