UNIPROT:P41181 - FACTA Search

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

The nature of the paracellular pathway of the rabbit cortical collecting duct (CCD) was examined under conditions designed to eliminate all cellular ion transport. Transcellular conductive pathways were blocked by addition of amiloride and Ba2+ to the perfusate. Cl self-exchange was eliminated by removing Cl from the bath solution, and HCO3 transport was eliminated by omitting HCO3 and CO2 from the solutions. The residual transepithelial conductance (GT) and radioisotopic tracer flux under these conditions probably occur via the paracellular pathway. The GT measured in nontransporting CCD bathed in NaCl solutions was 1.1-1.2 mS/cm2. When Na or Cl was replaced by a less mobile ion, the GT decreased by an amount commensurate with the decrease in solution conductivity. The Na-to-Cl permeability ratio determined by NaCl dilution voltages ranged from 0.55 to 0.82. An independent estimate of paracellular selectivity was obtained by comparing the lumen-to-bath tracer rate coefficients for Na (kNa) and Cl (kCl). The ratio kNa:kCl was 0.75. These observations suggest that the paracellular pathway displays a Na:Cl permselectivity not substantially different from the ratio of their mobilities in water (0.65). Additional experiments demonstrated that the summed partial ionic conductances of Na and Cl calculated from the tracer fluxes were in close agreement with the measured GT. We conclude that the paracellular conductance of CCD is nonselective in character and approximately 1-2 mS/cm2 in magnitude.
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PMID:Characteristics of the paracellular pathway of rabbit cortical collecting duct. 317 55

To assess the intrinsic effects of treatment with furosemide on free-water excretion in patients with chronic renal failure, two groups of patients with and without replacement of diuretic-induced salt losses have been studied. Furosemide therapy was administered for 1 week during constant sodium intake (100 mEq/day). In neither of the groups did furosemide cause hyponatremia, while it did decrease the urine to plasma osmolality ratio, an effect lasting even when the diuretic effect was exhausted. During water diuresis, furosemide decreased the fractional sodium reabsorption in diluting segments but not the absolute rate of the free-water generation (CH2O). Presumably the expected decrease of CH2O was masked by the increased distal delivery of tubular fluid mainly due to an additional effect of the diuretic on the proximal tubule. The hypotonicity of urine after furosemide treatment may be secondary to the dissipation of medullary hypertonicity, caused by furosemide, in the condition of decreased water permeability of the collecting duct due to uremic disease.
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PMID:Effects of furosemide therapy on free-water excretion in uremic patients. 323 71

Recent classifications of the several pathophysiologic types of distal renal tubular acidosis (secretory, voltage dependent, and gradient) have been based on the response of acidification parameters to a series of provocative maneuvers in vivo and in vitro. A reduction in the difference in urine and blood CO2 tension during bicarbonate loading (U-B pCO2 gradient), a widely applied parameter, has been employed as an index of reduced distal nephron proton secretion. This study was designed to test the validity of the U-B pCO2 gradient in a variety of experimental models of distal renal tubular acidosis by measuring and comparing disequilibrium pH (a direct technique to detect H+ secretion in situ) with the pCO2 in the papillary collecting duct of the rat in vivo during bicarbonate loading. Chronic amiloride, lithium chloride, and amphotericin-B administration, and the post-obstructed kidney models were employed. Amiloride resulted in an acidification defect which did not respond to sulfate infusion (urine pH = 6.15 +/- 0.08), and was associated with an obliteration of the acid disequilibrium pH (-0.26 +/- 0.05- -0.08 +/- 0.03) and reduction in papillary pCO2 (116.9 +/- 3.2 - 66.9 +/- 2.5 mmHg). The defect induced by lithium administration responded to Na2SO4 (urine pH = 5.21 +/- 0.06) but was similar to amiloride with respect to the observed reduction in disequilibrium pH (-0.04 +/- 0.02) and pCO2 (90.3 +/- 3.0 mmHg). The post-obstructed kidney model was characterized by an abnormally alkaline urine pH unresponsive to sulfate (6.59 +/- 0.06) and a reduction in disequilibrium pH (+0.02 +/- 0.06) and pCO2 (77.6 +/- 3.6 mmHg). Amphotericin-B resulted in a gradient defect as characterized by excretion of an acid urine after infusion of sodium sulfate (5.13 +/- 0.06). Unlike other models, however, amphotericin-B was associated with a significant acid disequilibrium pH (-0.11 +/- 0.05) and an appropriately elevated urine pCO2 (119.8 +/- 6.4 mmHg) which did not differ from the respective values in control rats. Thus, these findings support the use of the U-B pCO2 as a reliable means of demonstrating impaired distal nephron proton secretion in secretory and voltage-dependent forms of distal renal tubular acidosis (RTA) and supports the view that proton secretion is not impaired in gradient forms of distal RTA.
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PMID:Validation of the difference in urine and blood carbon dioxide tension during bicarbonate loading as an index of distal nephron acidification in experimental models of distal renal tubular acidosis. 392 66

1. Cortical collecting ducts were dissected from slices of rabbit kidney, then perfused in vitro.2. Transtubular electrical potentials were measured before and after abrupt changes in peritubular fluid pH.3. Variation in peritubular fluid pH, induced either by alteration in HCO(3) (-) concentration or in H(2)PO(4) (-)/HPO(4) (2-) ratio, produced biphasic responses in potential. Thus, reduction in pH caused an immediate fall, and then a prolonged and marked rise, in transtubular potential. The converse occurred on raising the pH.4. Variation in luminal fluid pH between pH 4.85 and pH 7.35 did not alter this pattern of response.5. In contrast to the above, reduction of peritubular fluid pH by elevation of P(CO2) produced either no effect or a decrease in transtubular potential.6. The transtubular potential of the cortical collecting duct appears to be a function of the pH gradient across some as yet unidentified part of the wall of the duct.
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PMID:Peritubular pH and transtubular potentials in isolated perfused cortical collecting ducts of rabbit kidney. 501 64

The collecting duct system is a major site of ammonia addition to the tubule fluid. To study the mechanisms involved, we measured total ammonia and total CO2 transport in isolated, perfused cortical collecting ducts (CCD) from deoxycorticosterone-(DOC) treated rabbits. Perfusate and bath solutions contained 25 meq/liter HCO3 and 4 mM total ammonia. Net fluid transport was not significantly different from zero. Net secretion of total CO2 occurred in all tubules (mean collected concentration, 44.2 mM). Despite bicarbonate secretion, there was net secretion of total ammonia (mean collected concentration, 6.4 mM). There was no detectable ammonia addition to the collected fluid when ammonia was excluded from the perfusate and bath, ruling out a major contribution from synthesis. Ouabain did not significantly affect net transport of total ammonia or total CO2. To test the hypothesis that an acid pH disequilibrium may lower the luminal pH enough to drive ammonia secretion by nonionic diffusion, we perfused CCD from DOC-treated rabbits with carbonic anhydrase (CA) (0.1 mg/ml). Without CA, there was net total ammonia secretion (-2.2 pmol X min-1 X mm-1) and net total CO2 secretion (-16.6 pmol X min-1 X mm-1). Luminal CA converted the net total ammonia secretion to net absorption (1.0 pmol X min-1 X mm-1) while the bicarbonate secretion persisted (-11.2 pmol X min X mm-1). We conclude that total ammonia secretion in these tubules occurs primarily by diffusion of NH3 and is dependent on a luminal acid pH disequilibrium.
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PMID:Mechanism of ammonia secretion by cortical collecting ducts of rabbits. 609 87

Eighty-four male white leghorn chickens were killed by CO2 gas to determine the type, rate, and sequence of postmortem microscopic changes in the kidneys of dry and wet intact carcasses. They were held at 29 or 18 C with 50% relative humidity for different times postmortem. Microscopic postmortem changes in the different segments of the nephron underwent a different rate and sequence of cellular changes. Cellular changes occurred earlier at 29 C than at 18 C and earlier in chickens not wetted with detergent solution. The decrease in body temperature of wetted chickens over dry chickens was significant (P less than 0.05). The proximal convoluted tubule (PCT) underwent the earliest postmortem changes, followed by the distal convoluted tubule (DCT), collecting tubule (CT), medullary loop (ML), medullary collecting duct (MCD), and glomerulus. The PCT, DCT, and thin and thick segments of the ML underwent a sequential nuclear change of chromatin margination, progressive shrinkage, pyknosis, karyorrhexis, and karyolysis. Nuclei were pyknotic if cytoplasmic changes were severe. Primary karyorrhexis was the predominant feature of collecting tubules and ducts. As early as one hour after death, some PCT cells of all kidney sections were pyknotic, emphasizing that immediate tissue fixation was necessary for critical evaluation. By 9 and 18 hr postmortem, PCT of dry and wet chickens, respectively, held at 29 C had pyknotic and karyorrhectic nuclei with slight karyolysis and moderate to marked cytoplasmolysis that extended until 36 hr. At this time, DCT were hardly distinguishable because of loss of basophilia. Karyorrhectic nuclei were already evident in collecting tubules and ducts. At 48 hr postmortem, all tubular cells were non-nucleated with homogeneous, acidophilic cytoplasm. Basement membranes no longer stained with periodic acid-Schiff (PAS). Erythrocytes were pyknotic with unstained cytoplasm. Pyknotic glomeruli were first observed at 9 hr postmortem in dry chickens and 12 hr in wet chickens. Histologic appearance of dry chickens at 9 hr and wet chickens at 18 hr when held at 29 C was similar to that of dry chickens at 12 hr and wet chickens at 24 hr when held at 18 C, with minor differences in some tubular changes. At 18 C, pyknotic glomeruli appeared by 6 hr in dry chickens and 24 hr in wet chickens. Widespread bacterial invasion was noted at 72 hr in dry chickens and at 96 hr in wet chickens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Microscopic postmortem changes in kidneys of the domestic fowl. 620 7

Several theories have been advanced to explain the elevation in urinary PCO2 during bicarbonate loading and include: (a) H+ secretion, (b) countercurrent system for CO2, (c) the "ampholyte" properties of bicarbonate, and (d) mixing of urine of disparate bicarbonate and butter concentrations. In this study microelectrodes were used to measure in situ and equilibrium pH (pHis and pHeq) and PCO2 in control and bicarbonate loaded rats before and after infusion of carbonic anhydrase. The disequilibrium pH method (pHdq = pHis - pHeq) was used to demonstrate H+ secretion. Control rats excreting an acid urine (pH = 6.04 +/- 0.06) failed to display a significant disequilibrium pH at the base (BCD), or tip (TCD) of the papillary collecting duct. Urine pH (7.54 +/- 0.12), and urine to blood (U-B) PCO2 increased significantly during NaHCO3 loading while PCO2 at the BCD and TCD also increased (95 +/- 4 and 122 +/- 4). Furthermore, an acid disequilibrium pH was present at both the BCD and TCD (-0.42 +/- 0.04 and -0.36 +/- 0.03) and was obliterated by carbonic anhydrase. Comparison of the PCO2 in the BCD or TCD with the adjacent vasa recta revealed similar values (r = 0.97). It is concluded that H+ secretion by the collecting duct into bicarbonate containing fluid with delayed dehydration of H2CO3, is the most likely determinant of the U-B PCO2 in alkaline urine. Similar values for PCO2 in the collecting duct and the adjacent vasa recta suggests trapping of CO2 in the medullary countercurrent system. The rise in PCO2 occurs both along the collecting duct and after exit from the papilla.
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PMID:Hydrogen ion secretion by the collecting duct as a determinant of the urine to blood PCO2 gradient in alkaline urine. 627 13

During a bicarbonate diuresis, final urine Pco2 considerably exceeds systemic Pco2, an effect thought to reflect the postpapillary delayed dehydration of carbonic acid. To test this explanation, Pco2 tensions along the inner medullary collecting duct (IMCD) of bicarbonate-loaded rats were measured directly using Pco2 microelectrodes. With systemic Pco2 held at 40 mm Hg, IMCD Pco2 exceeded systemic Pco2 in every measurement by an average of 20 to 30 mm Hg. A significant increment in Pco2 was seen between 50% IMCD length and the papilla tip. During the infusion of carbonic anhydrase, IMCD Pco2 was reduced but not to systemic levels. Finding elevated Pco2 along the terminal IMCD deemphasizes the importance of postpapillary delayed dehydration and suggests the possibility that bicarbonaturia is associated with papillary accumulation of carbon dioxide.
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PMID:Elevated urinary PCO2 in the rat: an intrarenal event. 629 Jul 41

The purpose of this study was to determine and compare pH, PCO2, and fractional bicarbonate delivery in both superficial and juxtamedullary nephrons by microelectrode techniques and microcalorimetry in the rat in vivo in order to define more clearly the role of deeper nephron segments in urinary acidification. Values for pH and total CO2 concentration ([tCO2]) at the bend of Henle's loop (LOH) (7.39 +/- 0.04 units and 20.5 +/- 1.5 mM) were significantly greater and the PCO2 was significantly less (36.6 +/- 1.5 mmHg) than values for these same parameters in the superficial late proximal tubule (LPT) (6.78 +/- 0.03 units, 8.1 +/- 1.2 mM, and 63.2 +/- 1.0 mmHg, P less than 0.001). The fraction of filtered bicarbonate delivered to the LPT and LOH did not differ, however (12.2 +/- 2.5 vs. 9.0 +/- 0.8%). The pH and PCO2 values in the late distal tubule (6.59 +/- 0.04 units and 64.0 +/- 1.3 mmHg) were significantly greater than at the base (6.24 +/- 0.07 units and 34.5 +/- 1.5 mmHg) and tip (6.12 +/- 0.03 units and 35.2 +/- 1.2 mmHg) of the papillary collecting duct. The [tCO2] in the LOH and an adjacent vasa recta was compared and did not differ significantly (20.5 +/- 1.5 vs. 21.2 +/- 1.3 mM, P greater than 0.05). In summary, we have demonstrated significant alkalinization of tubule fluid in the deep LOH as a result of water abstraction and CO2 diffusion from the nephron. Our results suggest that a spontaneous disequilibrium pH may not exist in the LOH. Furthermore, similar values for [tCO2] in vasa recta and the LOH suggest that passive HCO-3 reabsorption in the thin ascending limb of Henle would be unlikely and does not contribute to the "loop" component of bicarbonate reabsorption.
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PMID:Comparison of acidification parameters in superficial and deep nephrons of the rat. 640 28

The present experiments were designed to localize the sites of carbonic anhydrase-independent bicarbonate reabsorption in the rat kidney and to examine some of its mechanisms. Young Munich-Wistar rats were studied using standard cortical and papillary free-flow micropuncture techniques. Total CO2 (tCO2) was determined using microcalorimetry. In control rats both superficial and juxtamedullary proximal nephrons reabsorbed approximately 95% of the filtered load of bicarbonate. The administration of acetazolamide (20 mg/kg body weight [bw]/h) decreased proximal reabsorption to 65.6% of the filtered load in superficial nephrons (32% was reabsorbed by the proximal convoluted tubule while 31.7% was reabsorbed by the loop segment), and to 38.4% in juxtamedullary nephrons. Absolute reabsorption of bicarbonate was also significantly higher in superficial than in juxtamedullary nephrons after administration of acetazolamide (727 +/- 82 vs. 346 +/- 126 pmol/min; P less than 0.05). The infusion of amiloride (2.5 mg/kg bw/h) to acetazolamide-treated rats increased the fractional excretion of bicarbonate as compared with animals treated with acetazolamide alone (34.9 +/- 1.9 vs. 42.9 +/- 2.1%; P less than 0.01), and induced net addition of bicarbonate between the superficial early distal tubule and the final urine (34.8 +/- 3.0 vs. 42.9 +/- 2.1%; P less than 0.05). Amiloride at this dose did not affect proximal water or bicarbonate transport; our studies localize its site of action to the terminal nephron. Vasa recta (VR) plasma and loop of Henle (LH) tubular fluid tCO2 were determined in control and acetazolamide-treated rats in order to identify possible driving forces for carbonic anhydrase-independent bicarbonate reabsorption in the rat papilla. Control animals showed a tCO2 gradient favoring secretion (LH tCO2, 7.4 +/- 1.7 mM vs. VR tCO2, 19.1 +/- 2.3 mM; P less than 0.005). Acetazolamide administration reversed this chemical concentration gradient, inducing a driving force favoring reabsorption of bicarbonate (LH tCO2, 27.0 +/- 1.4 mM vs. VR tCO2, 20.4 +/- 1.0 mM; P less than 0.005). Our study shows that in addition to the superficial proximal convoluted tubule, the loop segment and the collecting duct show acetazolamide-insensitive bicarbonate reabsorption. No internephron heterogeneity for bicarbonate transport was found in controls. The infusion of acetazolamide, however, induced significant internephron heterogeneity for bicarbonate reabsorption, with superficial nephrons reabsorbing a higher fractional and absolute load of bicarbonate than juxtamedullary nephrons. We think that the net addition of bicarbonate induced by amiloride is secondary to inhibition of voltage-dependent, carbonic anhydrase-independent bicarbonate reabsorption at the level of the collecting duct, which uncovers a greater delivery of carbonate from deeper nephrons to the collecting duct. Finally, our results suggest that carbonic anhydrase-independent bicarbonate reabsorption is partly passive, driven by favorable chemical gradients in the papillary tubular structures, and partly voltage-dependent, in the collecting duct.
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PMID:Internephron heterogeneity for carbonic anhydrase-independent bicarbonate reabsorption in the rat. 642 64

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