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

The collecting duct of the mammalian kidney is involved in urine acidification. Recent studies in the turtle bladder suggest that hydrogen ion secretion in response to elevated CO2 is regulated by insertion of hydrogen pumps into the luminal membrane of the mitochondria-rich cells. Because intercalated cells of the collecting duct are structurally similar to mitochondria-rich cells of the amphibian bladder, we studied the rat outer medullary collecting duct (OMCD) during respiratory acidosis to determine whether changes compatible with hydrogen ion secretion occur in the intercalated cells. Rats were studied during normal acid-base conditions and after 4-5 h of respiratory acidosis. After collection of physiologic data, the kidneys were fixed by in vivo perfusion and processed for electron microscopy. No changes were observed in the principal cells of the OMCD. Morphometric analysis revealed a significant increase in the surface density of the apical plasma membrane and a decrease in the number of tubulovesicular profiles in the apical region of the intercalated cells throughout the OMCD with respiratory acidosis. There were no changes in surface density of the basolateral membrane. These findings suggest that in response to respiratory acidosis there is transport of membrane from the tubulovesicular membrane compartment to the apical plasma membrane of the intercalated cells.
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PMID:Cellular response to acute respiratory acidosis in rat medullary collecting duct. 666 Feb 92

To determine whether chloride-depletion metabolic alkalosis (CDA) can be corrected by provision of chloride without volume expansion or intranephronal redistribution of fluid reabsorption, CDA was produced in Sprague-Dawley rats by peritoneal dialysis against 0.15 M NaHCO3; controls (CON) were dialyzed against Ringer's bicarbonate. Animals were infused with isotonic solutions containing the same Cl and total CO2 (tCO2) concentrations as in postdialysis plasma at rates shown to be associated with slight but stable volume contraction. During the subsequent 6 h, serum Cl and tCO2 concentrations remained stable and normal in CON and corrected towards normal in CDA; urinary chloride excretion was less and bicarbonate excretion greater than those in CON during this period. Micropuncture and microinjection studies were performed in the 3rd h after dialysis. Plasma volumes determined by 125I-albumin were not different. Inulin clearance and fractional chloride excretion were lower (P less than 0.05) in CDA. Superficial nephron glomerular filtration rate determined from distal puncture sites was lower (P less than 0.02) in CDA (27.9 +/- 2.3 nl/min) compared with that in CON (37.9 +/- 2.6). Fractional fluid and chloride reabsorption in the proximal convoluted tubule and within the loop segment did not differ. Fractional chloride delivery to the early distal convolution did not differ but that out of this segment was less (P less than 0.01) in group CDA. Urinary recovery of 36Cl injected into the collecting duct segment was lower (P less than 0.01) in CDA (CON 74 +/- 3; CDA 34 +/- 4%). These data show that CDA can be corrected by the provision of chloride without volume expansion or alterations in the intranephronal distribution of fluid reabsorption. Enhanced chloride reabsorption in the collecting duct segment, and possibly in the distal convoluted tubule, contributes importantly to this correction.
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PMID:Segmental chloride and fluid handling during correction of chloride-depletion alkalosis without volume expansion in the rat. 669 Apr 86

To directly characterize acidification by the collecting duct, we developed pH and PCO2 microelectrodes suitable for microcatheterization of the inner medullary collecting duct (IMCD). In saline-infused control rats apparent in situ pH fell significantly along the IMCD, from 5.95 at 60% length to 5.49 at the papilla tip. Luminal PCO2 averaged 34 +/- 1 mmHg and PD averaged +3 mV. In rats acutely infused with 0.1 N HCl, apparent in situ pH also decreased significantly from 5.56 to 5.28, PD averaged +2 mV, and luminal PCO2 31 +/- 1 mmHg. The luminal PCO2 of HCl-infused rats was significantly less than controls and both levels were significantly below arterial PCO2. Corroborating the in situ pH profiles, equilibrium pH measured on collected IMCD samples also decreased significantly with percent length. In samples measured in situ and at equilibrium, a small but significant acid disequilibrium pH ws seen in both groups. We interpret these results to indicate that the IMCD actively participates in distal acidification. It is proposed that acidification by the IMCD is predominantly mediated by hydrogen ion secretion which simultaneously acidifies luminal fluid and generates a cellular sink for CO2, thereby inducing an acid disequilibrium pH by two mechanisms.
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PMID:pH and PCO2 profiles of the rat inner medullary collecting duct. 679 82

The present study was designed to characterize bicarbonate (total CO2) reabsorption in the papillary collecting duct of the kidney of the Munich-Wistar rat when total CO2 delivery to this segment was increased by the systemic infusion of a bicarbonate-rich solution. Additional studies examined the effect of the systemic administration of acetazolamide, a carbonic anhydrase inhibitor, on total CO2 reabsorption. Employing free-flow micropuncture techniques, tubular fluid samples were obtained from the base and tip of the exposed papilla and subsequently analyzed for total CO2 and inulin. Total CO2 reabsorption increased in a linear fashion, approximating 34% of that delivered to the base, as total CO2 delivery increased from 3 to 20% of the filtered load. When examined at comparable absolute rates of total CO2 delivery (mumol/min) to the papillary collecting duct, acetazolamide administration resulted in marked inhibition of total CO2 reabsorption. The results of these studies suggest that the papillary collecting duct of the rat kidney possesses a significant capacity for reabsorption of total CO2 and that this reabsorption is diminished by the administration of acetazolamide.
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PMID:Bicarbonate reabsorption in the papillary collecting duct: effect of acetazolamide. 680 6

The acidification of the urine within the distal tubule of Amphiuma means was studied with micropuncture techniques. Antimony microelectrodes calibrated in vivo were used for measuring the intratubular pH and samples were taken for the determination of Na+- and Cl- -concentrations and for determining buffer lines within the HCO-3-CO2 buffer system. The TF/P Na+ was used as a relative length determinator and a significant acidification along the length of the tubule was found. The pH in the tubule was more acid than samples equilibrated at blood PCO2. This disequilibrium can be described in terms of an imbalance within the Henderson-Hasselbach formula or/and as a PCO2-gradient across the tubular wall. The calculated PCO2-gradient was found to be correlated to the arterial PCO2 and the acidification to the arterial pH. The greatest pH-gradient is generated in the collecting duct and in the bladder.
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PMID:Acidification in the distal tubule of the Amphiuma kidney. 688 Jul 93

Renal function was investigated in rats 3 d or 4 wk after an injection of 2-bromoethylamine hydrobromide (BEA) 40-125 mg/kg body weight. Animals developed necrosis of renal papillary structures other than collecting ducts (subtotal renal papillary necrosis) (RPN) or necrosis of all structures in the distal papilla, including collecting ducts (total RPN). Glomerular filtration rate (GFR) was reduced in animals with total RPN (667 +/- SD 168 microliters/min/100 g body weight, n = 5) in comparison with controls (1065 +/- 103, n = 5; P less than 0.001) but was unimpaired in animals with subtotal RPN (1162 +/- 200, n = 4; P greater than 0.3). Maximum urinary osmolality (Umax) was significantly decreased in subtotal RPN (1241 +/- 388 mOsm/kg, n = 4) and in total RPN (626 +/- 293, n = 5) in comparison with controls (2216 +/- 293, n = 5). Free water reabsorption (TcH2O) was impaired in animals with total RPN but was not significantly reduced in the presence of subtotal RPN. Total RPN did not affect free water formation (CH2O). It is concluded that impaired TcH2O occurs in RPN because of the damage to the collecting duct, and not because of necrosis of the thin limbs juxtamedullary nephrons.
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PMID:Localization of medullary functional abnormalities in experimental papillary necrosis. 715 35

Utilization of classical clearance methodology for the determination of diuretic mechanism and site of action is based on four kinds of observations: (1) the effects of diuretic agents on the concentrating and diluting mechanism; (2) an analysis of the pattern of anionic excretion produced by the drug; (3) determination of the action of the agent on acid excretion and on acid-base status; (4) an evaluation of the effects of the diuretic on potassium excretion. Agents (such as acetazolamide) that act in the proximal convoluted tubule cause an enhancement of solute-free water generation (CH2O), induce a phosphaturia and an increase in bicarbonate excretion, alkalinize the urine, and cause a kaliuresis. Those agents which inhibit sodium chloride transport in the loop of Henle (for example, furosemide and ethacrynic acid) reduce both CH2O and the abstraction of tubular water from the collecting duct (TCH2O). They are the most potent natriuretic agents currently available, causing increments in the excretion of sodium in the urine of 15 to 25 per cent of filtered load. Those drugs which act in the early portion of the distal convolution (the thiazides, metolazone) reduce CH2O modestly or not at all and have no effect on TCH2O. They are capable of increasing urinary sodium by 5 to 8 per cent of the filtered load. The special-purpose agents such as triamterene and spironolactone are only mildly effective as natriuretic agents. While they augment fractional sodium excretion by only 2 to 3 per cent, they are useful because of their capacity to reduce urinary potassium excretion, either by a direct renal tubular effect (triamterene) or by competitive inhibition of aldosterone (spironolactone).
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PMID:Sites and mechanisms of action of diuretics in the kidney. 733 66

The renal concentrating ability of Fischer 344 rats was studied at 23 and 4 mo of age. Maximum urine concentration after 40 h of dehydration with or without vasopressin injection was significantly lower (P less than 0.01) in old (2,550 +/- 70 and 2,363 +/- 107 mosmol/kg H2O2, respectively) vs. young (3,242 +/- 50 and 3,162 +/- 50 mosmol/kg H2O, respectively) rats. Free water reabsorption (TcH2O/GFR) rose progressively as a function of osmolar clearance, and at similar values of distal solute delivery TcH2O was clearly reduced in the old group. Free water formation (CH2O/GFR) rose linearly as a function of urine flow and was not different between old and young rats. Glomerular filtration rate was also not different between age groups under the conditions studied. Nonurea (sodium + potassium + ammonium) x 2 and urea solute concentrations as well as total calculated osmolality in the cortex, outer medulla, or inner medulla were not different between age groups. Because the indices of ascending limb solute delivery and transport and the solute gradient for water reabsorption were similar, we conclude that the concentrating defect in aged rats is most likely secondary to a decrease in water permeability along the collecting duct.
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PMID:Urinary concentrating defect in the aged rat. 746 99

Renal correction of chloride-depletion alkalosis (CDA) by chloride replacement results in bicarbonate secretion in the cortical collecting duct (CD) and urinary bicarbonate excretion. To assess the participation of the more distal segments of the CD, we determined net total CO2 transport in the outer medullary (OMCD), initial (IMCDi) and terminal (IMCDt) inner medullary CD segments obtained from Sprague-Dawley rats with normal acid-base balance (NML) or with CDA produced by peritoneal dialysis. Tubules were bathed and perfused with isotonic solutions containing Cl 110 mM and HCO, 25 mM. Net total CO2 transport was decreased in all segments: OMCD 22.1 +/- 4.2 to 9.2 +/- 2.0; IMCDi 38.1 +/- 4.6 to 9.3 +/- 1.7; IMCDt 6.7 +/- 1.2 to -0.5 +/- 0.4 pmol/min/mm tubule length. Perfusion rates, tubule lengths, and transepithelial voltages did not differ between groups in any segment. These data show that all CD segments beyond the cortical segment decrease bicarbonate reabsorption during CDA. This permits the bicarbonate secreted by the cortical CD to be excreted, and is likely an important mechanism for the correction of CDA.
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PMID:Bicarbonate transport in collecting duct segments during chloride-depletion alkalosis. 756 91

At least two cortical collecting duct (CCD) intercalated cell populations mediate HCO3- secretion and reabsorption. The present study examined the membrane location of intercalated cell Cl-/base exchange activity and the axial distribution of CCD intercalated cells. CCD were studied using in vitro microperfusion in CO2/HCO3(-)-containing solutions; intracellular pH was measured using 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The A-type intercalated cell (A cell) and B-type intercalated cell (B cell) were identified functionally by the absence and presence of apical Cl-/HCO3- exchange activity, respectively. When a 0 mM Cl-, 0 mM HCO3- luminal solution was used, removal of Cl- from the peritubular solution caused intracellular alkalinization in all B cells. The alkalinization required neither extracellular Na+ nor changes in membrane potential. Peritubular 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (10(-4) M) inhibited A cell but not B cell basolateral Cl-/base exchange activity. In comparison to studies performed with a 0 mM Cl- 0 mM HCO3- luminal solution, the use of a 0 mM Cl-, 25 mM HCO3- luminal solution inhibited both the identification and the magnitude of B cell basolateral Cl-/base exchange activity. When CCD from the inner and outer cortex were separately studied, only 7% of outer CCD intercalated cells were A cells, whereas 93% were B cells. In contrast, in the inner CCD, 58% of intercalated cells were A cells and 42% were B cells. Under stop-flow conditions, outer CCD alkalinized the luminal fluid, whereas inner CCD acidified the luminal fluid. These results indicate that all CCD intercalated cells possess basolateral Cl-/base exchange activity; however, A cell and B cell basolateral Cl-/base exchange activity differs, at least in terms of sensitivity to DIDS. Furthermore, there is axial heterogeneity in both intercalated cell type and function.
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PMID:Distribution of Cl-/HCO3- exchange and intercalated cells in rabbit cortical collecting duct. 781 Jul 3


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