PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Kidney Tubules, Collecting”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1988

[The role of the ultrastructure of the intercalated cells of the kidney collecting tubules in rats in secreting hydrogen ions].

Upon experimental metabolic acidosis in rats, induced by a long-term per os administration of a 10% ammonium chloride solution, elevation of titred acidity and ammonium level in rat's urea was registered, in addition to an increased number of intercalated cells in collecting tubules of kidney medullar zone, where the highest carboanhydrase activity occurred. The structural and functional unit of the intercalated cell is a smooth vesicle having presumable H+-,K+-translocating exchange pump within its membrane. The vesicles accumulating gradually H-ions move to the apical cell membrane to release their content by exocytosis into the tubule space. Under H+-ion hypersecretion, upon experimental acidosis, the vesicle membrane is built into the apical plasma membrane, where H+,K+-exchange occurs, thus intensity of this process increasing. The apical plasma membrane of the cell extends its surface at the expense of intracellular canaliculi that are formed.

Acid-Base Equilibrium↗
PubMed1991

Transcellular water flow modulates water channel exocytosis and endocytosis in kidney collecting tubule.

The regulation of osmotic water permeability (Pf) by vasopressin (VP) in kidney collecting tubule involves the exocytic-endocytic trafficking of vesicles containing water channels between an intracellular compartment and apical plasma membrane. To examine effects of transcellular water flow on vesicle movement, Pf was measured with 1-s time resolution in the isolated perfused rabbit cortical collecting tubule in response to addition and removal of VP (250 microU/ml) in the presence of bath greater than lumen (B greater than L), lumen greater than bath (L greater than B), and lumen = bath (L = B) osmolalities. With VP addition, Pf increased from 12 to 240-270 x 10(-4) cm/s (37 degrees C) in 10 min. At 1 min, Pf was approximately 70 x 10(-4) cm/s for B greater than L, L greater than B, and L = B conditions. At later times, Pf increased fastest for L greater than B and slowest for B greater than L osmolalities; at 5 min, Pf was 250 x 10(-4) cm/s (L greater than B) and 158 x 10(-4) cm/s (B greater than L). With VP removal, Pf returned to pre-VP levels at the fastest rate for B greater than L and the slowest rate for L greater than B osmolalities; at 30 min, Pf was 65 x 10(-4) cm/s (B greater than L) and 183 x 10(-4) cm/s (L greater than B). For a series of osmotic gradients of different magnitudes and directions, the rates of Pf increase and decrease were dependent upon the magnitude of transcellular volume flow; control studies showed that paracellular water flux, asymmetric transcellular water pathways, or changes in cell volume could not account for the data. VP-dependent endocytosis was measured by apical uptake of rhodamine-dextran; in paired studies where the same tubule was used for + and - gradients, B greater than L and L greater than B osmolalities gave 168% and 82% of uptake measured with no gradient. In contrast, endocytosis in proximal tubule was not dependent on gradient direction. These data provide evidence that transcellular volume flow modulates the vasopressin-dependent cycling of vesicles containing water channels, suggesting a novel driving mechanism to aid or oppose the targeted, hormonally directed movement of subcellular membranes.

Animals↗
PubMed1993

Cloning and expression of apical membrane water channel of rat kidney collecting tubule.

Concentrating urine is mandatory for most mammals to prevent water loss from the body. Concentrated urine is produced in response to vasopressin by the transepithelial recovery of water from the lumen of the kidney collecting tubule through highly water-permeable membranes. In this nephron segment, vasopressin regulates water permeability by endo- and exocytosis of water channels from or to the apical membrane. CHIP28 is a water channel in red blood cells and the kidney proximal tubule, but it is not expressed in the collecting tubule. Here we report the cloning of the complementary DNA for WCH-CD, a water channel of the apical membrane of the kidney collecting tubule. WCH-CD is 42% identical in amino-acid sequence to CHIP28. WCH-CD transcripts are detected only in the collecting tubule of the kidney. Immunohistochemically, WCH-CD is localized to the apical region of the kidney collecting tubule cells. Expression of WCH-CD in Xenopus oocytes markedly increases osmotic water permeability. The functional expression and the limited localization of WCH-CD to the apical region of the kidney collecting tubule suggest that WCH-CD is the vasopressin-regulated water channel.

Amino Acid Sequence↗
PubMed1980

Similarities of membrane structure in freeze-fractured Xenopus laevis kidney collecting tubule and urinary bladder.

The collecting tubule of Xenopus laevis kidney is formed of two main types of cell: the socalled flask cells (or mitochondria-rich cells) and the remaining, more cuboidal epithelial cells. It has previously been shown that the flask-cell plasma membrane contains a population of elongated intramembrane particles similar to those found in mitochondria-rich cells of the toad bladder. It is now clear that the structure of the apical membrane of the remaining epithelial cells of the collecting duct is similar to the apical membrane of the amphibian urinary bladder granular cells. The P-face of the apical membrane has relatively few particles, whereas the E-face has many more. The E-face particles are of large diameter (16 nm), and many of them have an apical dense spot, which may represent a pit or depression in the particle. Such particles are not found on the lateral E-face below the level of the tight junctions. At the present time, the functional significance of these particles is unknown, but since vasopressin fails to elicit a hydrosmotic response in Xenopus laevis they are probably not involved in transepithelial water permeability. The fact that the different membrane specializations which characterize these mitochondria-rich and non-mitochondria-rich cells are found both in the bladder and the collecting tubule suggests that, at least in Xenopus, the 2 epithelia may share some common functions at the level of the apical membranes of their constituent cells.

Animals↗
PubMed1988

Rapid development of vasopressin-induced hydroosmosis in kidney collecting tubules measured by a new fluorescence technique.

The pre-steady-state kinetics of the vasopressin-induced increase in collecting tubule osmotic water permeability (Pf) has been measured by a new fluorescence technique. Isolated cortical collecting tubules (CCT) from rabbit kidney were perfused with physiological buffers containing the impermeant fluorophores fluorescein sulfonate (FS) and pyrenetetrasulfonic acid (PTSA). Tubules were subject to a 120 mOsm bath-to-lumen osmotic gradient in the presence and absence of 250 microU/ml vasopressin. The magnitude of transepithelial volume flow was determined from the self-quenching of FS, or from the ratio of PTSA/FS fluorescence, measured at 380 nm excitation and 420 +/- 10 nm (PTSA) and greater than 530 nm (FS) emission wavelengths. Pf was calculated from the magnitude of transepithelial volume flow, lumen and bath osmolarities, lumen perfusion rate, and tubule geometry. The instrument response time for a change in bath osmolality was less than 3 s. At 37 degrees C, CCT Pf was (in units of cm/s x 10(4] 13 +/- 2 (mean +/- SE, 16 tubules) before, and 227 +/- 10 after addition of vasopressin to the bath. CCT Pf began to increase in 23 +/- 3 s after vasopressin addition and was half-maximal after 186 +/- 20 s. At 23 degrees C, Pf was 9 +/- 1 (seven tubules) before, and 189 +/- 12 after vasopressin addition. Pf began to increase in 40 +/- 4 s and was half-maximal after 195 +/- 35 s. After vasopressin removal from the bath, Pf decreased to its baseline value with a half-time of 14 min. These results establish a direct fluorescence method to monitor instantaneous transepithelial Pf in perfused tubules and show a very fast stimulation of CCT Pf in response to vasopressin.

Animals↗
PubMed1989

Detection of human autoantibody against intercalated cells of kidney-collecting tubule.

Serum from a 24-year-old woman with a history of habitual abortions was examined for autoantibodies by indirect immunofluorescence microscopy. Fluorochrome-labelled antibodies to IgG revealed cytoplasmic staining of single cells in rat kidney collecting and connecting tubules. An identical staining pattern was reproducibly obtained in human and rabbit kidney, pointing to a cytoplasmic antigen concentrated in the apical pole of these cells. Lectin-binding histochemistry and immunohistochemical experiments using markers for different cell populations of the renal collecting tubule by double immunofluorescence technique, identified the cells recognized by the autoantibody as intercalated cells (ICC). Remarkably, this autoantibody reacted with a different antigen from those described to date in ICC, as evidenced by distribution and intracellular localization. The pattern of immunostaining suggests that all ICC are recognized in total rather than only one subpopulation. The connection between habitual abortions and this novel autoantibody are discussed.

Abortion, Habitual↗
PubMed1999

[Morphometric analysis of the effects of vasopressin in the rat kidney collecting tubules].

A significant increase in the water permeability was found in the rat outer medullary collecting duct (OMCD) cells in presence of 10-7M of vasopressin. The latter caused a decrease in the OMCD cell volume in isoosmotic medium in adult rats. In pups, the water permeability of the OMCD cells was very high. Vasopressin seems to be unable to decrease the cell volume of the OMCD cells in pups which suggests an immaturity of the cell transduction mechanism.

Aging↗
PubMed2002

[Effect of dehydration and dDAVP on water permeability of basolateral membranes of epithelial cells in the kidney collecting tubules].

Water permeability of the outer medullary collecting duct's (OMCD) basolateral membrane was determined in vitro in the tubules isolated from hyperhydrated or dehydrated Wistar rats. Oil was injected into the lumen to block apical membrane water permeability. OMCD fragments underwent a hypoosmic shock (600/300 mOsm) and epithelial cells volume increased ad recorded with a digital camera. The latter's rate was used to calculate apparent water permeability of the membrane (Pf). Treatment of the tubules with Hg2Cl2 suppressed the water permeability. Water deprivation and dDAVP induced an increase in the basolateral water permeability. The data obtained suggest that the water permeability of the OMCD basolateral membrane may be stimulated by vasopressin and water deprivation.

Animals↗
PubMed1989

Pre-steady-state analysis of the turn-on and turn-off of water permeability in the kidney collecting tubule.

Water transport across the mammalian collecting tubule is regulated by vasopressin-dependent water channel insertion into and retrieval from the cell apical membrane. The time course of osmotic water permeability (Pf) following addition and removal of vasopressin (VP) and 8-Br-cAMP was measured continuously by quantitative fluorescence microscopy using an impermeant fluorophore perfused in the lumen. Cortical collecting tubules were subjected to a 120 mOsm bath-to-lumen osmotic gradient at 37 degrees C with 10-15 nl/min lumen perfusion and 10-20 ml/min bath exchange rate. With addition of VP (250 microU/ml), there was a 23 +/- 3 sec (SEM, n = 16) lag in which Pf did not change, followed by a rise in Pf (initial rate 1.4 +/- 0.2 x 10(-4) cm/sec2) to a maximum of 265 +/- 10 x 10(-4) cm/sec. With addition of 8-Br-cAMP (0.01-1 mM) there was an 11 +/- 2 sec lag. For [8-Br-cAMP] = 0.01, 0.1 and 1 mM, the initial rate of Pf increase following the lag was (units 10(-4) cm/sec2): 1.1 +/- 0.1, 1.2 +/- 0.1 and 1.7 +/- 0.3. Maximum Pf was (units 10(-4) cm/sec): 64 +/- 4, 199 +/- 9 and 285 +/- 11. With removal of VP, Pf decreased to baseline (12 x 10(-4) cm/sec) with a T1/2 of 18 min; removal of 0.1 and 1 mM 8-Br-cAMP gave T1/2 of 4 and 8.5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1991

Relationship between vasopressin-sensitive water transport and plasma membrane fluidity in kidney collecting tubule.

The role of plasma membrane fluidity in the regulation of kidney tubule water permeability has been uncertain. We have used new methods to image the fluorescence anisotropy of fluidity-sensitive fluorophores (Fushimi, Dix, and Verkman. Biophys. J. 57: 241-254, 1990) to quantitate membrane fluidity in cells of the vasopressin-sensitive cortical collecting tubule (CCT) and water-impermeable cortical thick ascending limb (CTAL). Isolated tubule segments from rabbit kidney were perfused in vitro, and apical or basolateral plasma membranes were stained with trimethylammonium diphenylhexatriene (TMA-DPH). TMA-DPH anisotropy (r) was imaged quantitatively by an epifluorescence microscope equipped with rotatable polarizers; TMA-DPH nanosecond lifetime (tau) was measured by flash-lamp excitation and gated photomultiplier detection. In CCT, apical membrane r (0.254 +/- 0.003) was similar to basolateral r (0.252 +/- 0.005). Serosal vasopressin at a dose that increased water permeability greater than 10-fold (250 microU/ml) did not affect apical membrane r (delta r = 0.002 +/- 0.003; 7 tubules). A 0.002 change in r was less than that produced by a 2 degrees C temperature variation. In CTAL, apical membrane r was 0.249 +/- 0.002, similar to r from basolateral membrane of proximal tubule (0.24), but much less than that of proximal tubule apical membrane (0.29). These results establish methodology to quantitate fluidity in intact kidney tubule segments and provide the first measurements of plasma membrane fluidity in CTAL and CCT. Our results suggest that regulation of bulk membrane fluidity in CCT apical membrane is not a component of the hydrosmotic action of vasopressin and that low apical membrane fluidity is not responsible for the low water and NH3 permeabilities in CTAL.

Animals↗
PubMed1988

Direct fluorescence measurement of diffusional water permeability in the vasopressin-sensitive kidney collecting tubule.

A fluorescence method has been developed for accurate and instantaneous measurement of transepithelial diffusional water permeability (Pd) in perfused kidney tubules based on the sensitivity of the fluorophore aminonapthelane trisulfonic acid (ANTS) to solution H2O/D2O content. The fluorescence of ANTS was 3.2-fold lower in an H2O buffer than in a D2O buffer. The response of ANTS fluorescence to a change in solution H2O/D2O content occurred in less than 1 ms and was due to a collisional quenching mechanism. Isolated cortical (CCT) and outer medullary (OMCT) collecting tubules from rabbit were perfused with an isosmotic D2O buffer at specified lumen flow rates (2-100 nl/min); tubules were bathed in isosmotic H2O or D2O buffers in which vasopressin (VP) could be added rapidly. Lumen fluorescence was monitored by quantitative epifluorescence microscopy at 380 +/- 5 nm excitation and greater than 530 emission wavelengths. Pd was determined from tubule geometry, lumen flow, ANTS fluorescence, and ANTS fluorescence vs. H2O/D2O calibration relation. The instrument response time for a change in bath H2O/D2O content was less than 4 s. At 37 degrees C, Pd values (mean +/- SE in cm/s x 10(4] were 6.4 +/- 1.0 (-VP, n = 9) and 14.3 +/- 1.1 (+250 microU/ml bath VP, n = 9) in the CCT, and 5.8 +/- 1.0 (-VP, n = 6) and 15.3 +/- 2.0 (+VP, n = 6) in the OMCT; at 23 degrees C, Pd was 5.1 +/- 0.6 (-VP, n = 4) and 7.8 +/- 0.6 (+VP, n = 4) in the CCT. In response to rapid addition of 250 micro U/ml vasopressin to the bath, CCT Pd remained unchanged for 71 +/- l0s (n = 9, 37 degree C) and 170 +/- 45 s (n = 4, 23 degree C); this was followed by a slow increase in Pd(TI/2 = 91 +/- 17 s, 37 degree C; 119 +/- 31 s, 23 degree C) to the new steady-state value. These results provide a new approach for study of transepithelial water transport in kidney tubules. Compared with 3H20 methods, the fluorescence method is superior in technical simplicity, time resolution, and accuracy. The improved time resolution is important for examination of the pre-steady-state kinetics of vasopressin-induced signalling events resulting in the hydroosmotic response.

Animals↗
PubMed1988

Endosomes from kidney collecting tubule cells contain the vasopressin-sensitive water channel.

The mechanism by which vasopressin rapidly and dramatically increases the water permeability of target epithelial cell membranes is thought to involve a cycle of exo- and endocytosis during which vesicles carrying 'water channels' are successively inserted into, and removed from the apical plasma membrane of epithelial cells. Clusters of intramembranous particles, visible by freeze-fracture electron microscopy and presumed to represent water channels, appear on apical membranes in parallel with increased transepithelial water flow. In the collecting duct, these clusters are located in clathrin-coated pits which are subsequently internalized. There has been no direct evidence, however, that subcellular membranes in vasopressin-sensitive epithelia contain functional water channels. In this report, we have used fluorophores that are sensitive to volume and do not pass through membranes to label and to measure directly the osmotic water permeability of endocytosed vesicles isolated from renal papilla. We present direct evidence that vasopressin induces the appearance of a population of endocytic vesicles whose limiting membranes contain water channels.

Animals↗
PubMed1993

H-K-ATPase in distal renal tubular acidosis: urinary tract obstruction, lithium, and amiloride.

In previous studies we suggested that urinary tract obstruction and chronic administration of lithium or amiloride were models of "voltage-dependent" distal renal tubular acidosis (DRTA). Subsequently, differences among these three models suggested that the pathogenesis was far more complex than we originally proposed. A recent study showed that H-adenosinetriphosphatase (H-ATPase) activity was decreased in all three experimental models. In the current experiments we examined the effect of 24-h unilateral ureteral obstruction (UUO) and chronic administration of amiloride and lithium on collecting tubule H-K-ATPase, the other renal H-ATPase enzyme. In the obstructed kidney, cortical collecting tubule (CCT) H-K-ATPase activity was enhanced by 73 +/- 10.0%, whereas the enzyme activity in medullary collecting tubule (MCT) was decreased by 67 +/- 5.4%. In the normal contralateral kidney, activities of H-ATPase, H-K-ATPase, and Na-K-ATPase were increased by approximately 30% in both CCT and MCT. Following amiloride (3 mg.kg-1.day-1 x 3 days ip), rats had normal acid-base status, slight hyperkalemia, and markedly elevated plasma aldosterone levels. Both CCT and MCT H-K-ATPase activities in amiloride-treated rats were unchanged. After LiCl (4 meq.kg-1.day-1 x 3 days ip), rats developed mild metabolic acidosis and had normokalemia and normal aldosterone status. CCT H-K-ATPase activity in lithium-treated rats was decreased by 64 +/- 8.8%, whereas the enzyme activity in MCT remained unchanged. Lithium in vitro (30 meq/l) inhibited CCT, but not MCT, H-K-ATPase activity, whereas amiloride had no effect on the enzyme activity. (ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1983

The fine structure of dark or intercalated cells from the distal and collecting tubules of avian kidneys.

Dark or intercalated cells were identified in the terminal portion of the distal tubules and in the intralobular collecting tubules of four species of birds. The morphological features of these cells varied only slightly from species to species and were very similar to cells found in topographically analogous regions of mammalian nephrons. Characteristic vesicles usually filled the apical region of the dark cells and were often in direct continuity with the apical plasma membrane which was frequently thrown into elaborate folds, microvilli and microplicae. Observations suggested that the cells might be involved in some form of cyclical secretory activity. The similarity in structure between avian and mammalian dark cells suggested that they might perform similar functions and that the study of avian cells might aid the elucidation of the mammalian cell function. The possible functions of the avian cells were discussed in relation to physiological studies in mammalian kidneys and it was suggested that they might be involved with proton and potassium pumping and control of urinary buffer concentrations.

Animals↗
PubMed1990

Binding of 3H-aldosterone and 3H-dexamethasone in primary monolayer cultures of kidney cortical collecting tubule (CCT) cells.

Specific binding of corticosteroids in cultured CCT cells was measured as a function of time, of temperature, of pH, and of concentration. Scatchard analysis revealed the existence of two species of binding sites for both, 3H-aldosterone type I A: KD = 2.3.10(-9) M, N = 33.10(-17) mol/10(4) cells; type I B: KD = 51.10(-9) M, N = 55.10(-17) mol/10(4) cells) and dexamethasone (type II A: KD = 4.7.10(-9) M, N = 2.3.10(17) mol/10(4) cells; type II B: KD = 22.10(-9) M, N = 6.5.10(-17) mol/10(4) cells). The data demonstrate that CCT cells in primary monolayer culture express corticosteroid binding sites similar to cells of the CCT in vivo.

Aldosterone↗