scholarly journals Apical extracellular calcium/polyvalent cation-sensing receptor regulates vasopressin-elicited water permeability in rat kidney inner medullary collecting duct.

1997 ◽  
Vol 99 (6) ◽  
pp. 1399-1405 ◽  
Author(s):  
J M Sands ◽  
M Naruse ◽  
M Baum ◽  
I Jo ◽  
S C Hebert ◽  
...  
Keyword(s):  
Water Permeability ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Extracellular Calcium ◽  
Polyvalent Cation ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Cation Sensing

Water permeability of apical and basolateral cell membranes of rat inner medullary collecting duct

1990 ◽  
Vol 259 (6) ◽  
pp. F986-F999 ◽  
Author(s):  
B. Flamion ◽  
K. R. Spring
Keyword(s):  
Water Flow ◽  
Water Permeability ◽  
Cell Membranes ◽  
Apical Membrane ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Volume Regulatory Decrease ◽  
Water Permeation ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

To quantify the pathways for water permeation through the kidney medulla, knowledge of the water permeability (Posmol) of individual cell membranes in inner medullary collecting duct (IMCD) is required. Therefore IMCD segments from the inner two thirds of inner medulla of Sprague-Dawley rats were perfused in vitro using a setup devised for rapid bath and luminal fluid exchanges (half time, t1/2, of 55 and 41 ms). Differential interference contrast microscopy, coupled to video recording, was used to measure volume and approximate surface areas of single cells. Volume and volume-to-surface area ratio of IMCD cells were strongly correlated with their position along the inner medullary axis. Transmembrane water flow (Jv) was measured in response to a variety of osmotic gradients (delta II) presented on either basolateral or luminal side of the cells. The linear relation between Jv and delta II yielded the cell membrane Posmol, which was then corrected for membrane infoldings. Basolateral membrane Posmol was 126 +/- 3 microns/s. Apical membrane Posmol rose from a basal value of 26 +/- 3 microns/s to 99 +/- 5 microns/s in presence of antidiuretic hormone (ADH). Because of amplification of basolateral membrane, the ADH-stimulated apical membrane remained rate-limiting for transcellular osmotic water flow, and the IMCD cell did not swell significantly. Calculated transcellular Posmol, expressed in terms of smooth luminal surface, was 64 microns/s without ADH and 207 microns/s with ADH. IMCD cells in anisosmotic media displayed almost complete volume regulatory decrease but only partial volume regulatory increase.

Heat stress protein-associated cytoprotection of inner medullary collecting duct cells from rat kidney

1993 ◽  
Vol 265 (3) ◽  
pp. F333-F341 ◽  
Author(s):  
S. C. Borkan ◽  
A. Emami ◽  
J. H. Schwartz
Keyword(s):  
Heat Stress ◽  
Thermal Injury ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Metabolic Effects ◽  
Lactate Dehydrogenase Activity ◽  
Inner Medullary Collecting Duct ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct

Although heat stress proteins (HSPs) mediate thermotolerance, the cellular targets of thermal injury and mechanisms of acquired cytoprotection are unknown. To describe the metabolic effects of hyperthermia and the potential mechanisms of thermotolerance, the following were measured in inner medullary collecting duct cells after a 43 degrees C and/or a 50 degrees C thermal insult: 1) state III mitochondrial respiration (SIII MR), 2) glycolytic rate, 3) lactate dehydrogenase activity, 4) membrane permeability, and 5) HSP 72 content. Compared with controls incubated at 37 degrees C, cells heated to 50 degrees C showed a 30 and 50% reduction in glycolysis and SIII MR, respectively. After heating to 50 degrees C, the cell membrane remained intact and immunoreactive HSP 72 was not detected. In contrast, heating to 43 degrees C induced accumulation of HSP 72 and transiently increased both SIII MR and glycolysis. In addition, prior exposure to 43 degrees C completely prevented the fall in SIII MR and glycolysis anticipated with a subsequent 50 degrees C insult. Cytoprotection gradually diminished over several days and correlated with the disappearance of HSP 72. Preservation of oxidative and anaerobic metabolism associated with HSPs may be important in developing resistance to thermal injury.

scholarly journals Transcriptional profiling of native inner medullary collecting duct cells from rat kidney

2008 ◽  
Vol 32 (2) ◽  
pp. 229-253 ◽  
Author(s):  
Panapat Uawithya ◽  
Trairak Pisitkun ◽  
Brian E. Ruttenberg ◽  
Mark A. Knepper
Keyword(s):  
Signal Intensity ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Transcriptional Profiling ◽  
High Signal ◽  
Inner Medullary Collecting Duct ◽  
Duct Cells ◽  
Collecting Duct Cells ◽  
Medullary Collecting Duct ◽  
V2 Vasopressin Receptor

Vasopressin acts on the inner medullary collecting duct (IMCD) in the kidney to regulate water and urea transport. To obtain a “parts list” of gene products expressed in the IMCD, we carried out mRNA profiling of freshly isolated rat IMCD cells using Affymetrix Rat 230 2.0 microarrays with ∼31,000 features; 7,913 annotated transcripts were found to be expressed above background in the IMCD cells. We have created a new online database (the “IMCD Transcriptome Database;” http://dir.nhlbi.nih.gov/papers/lkem/imcdtr/ ) to make the results publicly accessible. Among the 30 transcripts with the greatest signals on the arrays were 3 water channels: aquaporin-2, aquaporin-3, and aquaporin-4, all of which have been reported to be targets for regulation by vasopressin. In addition, the transcript with the greatest signal among members of the solute carrier family of genes was the UT-A urea transporter ( Slc14a2), which is also regulated by vasopressin. The V2 vasopressin receptor was strongly expressed, but the V1a and V1b vasopressin receptors did not produce signals above background. Among the 200 protein kinases expressed, the serum-glucocorticoid-regulated kinase ( Sgk1) had the greatest signal intensity in the IMCD. WNK1 and WNK4 were also expressed in the IMCD with a relatively high signal intensity, as was protein kinase A (β-catalytic subunit). In addition, a large number of transcripts corresponding to A kinase anchoring proteins and 14-3-3 proteins (phospho-S/T-binding proteins) were expressed. Altogether, the results combine with proteomics studies of the IMCD to provide a framework for modeling complex interaction networks responsible for vasopressin action in collecting duct cells.

Atrial natriuretic peptide and nitric oxide signaling antagonizes vasopressin-mediated water permeability in inner medullary collecting duct cells

2009 ◽  
Vol 297 (3) ◽  
pp. F693-F703 ◽  
Author(s):  
Jens Klokkers ◽  
Patrik Langehanenberg ◽  
Björn Kemper ◽  
Sebastian Kosmeier ◽  
Gert von Bally ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Plasma Membrane ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Water Permeability ◽  
Collecting Duct ◽  
Cell Swelling ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Atrial Natriuretic

AVP and atrial natriuretic peptide (ANP) have opposite effects in the kidney. AVP induces antidiuresis by insertion of aquaporin-2 (AQP2) water channels into the plasma membrane of collecting duct principal cells. ANP acts as a diuretic factor. An ANP- and nitric oxide (NO)/soluble guanylate cyclase (sGC)-induced insertion of AQP2 into the plasma membrane is reported from different models. However, functional data on the insertion of AQP2 is missing. We used primary cultured inner medullary collecting duct (IMCD) cells and digital holographic microscopy, calcein-quenching measurements, and immunofluorescence and Western blotting to analyze the effects of ANP and NO donors on AQP2 phosphorylation, membrane expression, and water permeability. While AVP led to acceleration in osmotically induced swelling, ANP had no effect. However, in AVP-pretreated cells ANP significantly decreased the kinetics of cell swelling. This effect was mimicked by 8-bromo-cGMP and blunted by PKG inhibition. Stimulation of the NO/sGC pathway or direct activation of sGC with BAY 58-2667 had similar effects to ANP. In cells treated with AVP, AQP2 was predominantly localized in the plasma membrane, and after additional incubation with ANP AQP2 was mostly localized in the cytosol, indicating an increased retrieval of AQP2 from the plasma membrane by ANP. Western blot analysis showed that ANP was able to reduce AVP-induced phosphorylation of AQP2 at position S256. In conclusion, we show that the diuretic action of ANP or NO in the IMCD involves a decreased localization of AQP2 in the plasma membrane which is mediated by cGMP and PKG.

scholarly journals Aldosterone Decreases Vasopressin-Stimulated Water Reabsorption in Rat Inner Medullary Collecting Ducts

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 967 ◽  
Author(s):  
Yanhua Wang ◽  
Fuying Ma ◽  
Eva L. Rodriguez ◽  
Janet D. Klein ◽  
Jeff M. Sands
Keyword(s):  
Direct Effect ◽  
Gene Transcription ◽  
Water Permeability ◽  
Collecting Duct ◽  
Osmotic Water Permeability ◽  
Water Reabsorption ◽  
Inner Medullary Collecting Duct ◽  
Urea Permeability ◽  
Osmotic Water ◽  
Medullary Collecting Duct

Aldosterone indirectly regulates water reabsorption in the distal tubule by regulating sodium reabsorption. However, the direct effect of aldosterone on vasopressin-regulated water and urea permeability in the rat inner medullary collecting duct (IMCD) has not been tested. We investigated whether aldosterone regulates osmotic water permeability in isolated perfused rat IMCDs. Adding aldosterone (500 nM) to the bath significantly decreased osmotic water permeability in the presence of vasopressin (50 pM) in both male and female rat IMCDs. Aldosterone significantly decreased aquaporin-2 (AQP2) phosphorylation at S256 but did not change it at S261. Previous studies show that aldosterone can act both genomically and non-genomically. We tested the mechanism by which aldosterone attenuates osmotic water permeability. Blockade of gene transcription with actinomycin D did not reverse aldosterone-attenuated osmotic water permeability. In addition to AQP2, the urea transporter UT-A1 contributes to vasopressin-regulated urine concentrating ability. We tested aldosterone-regulated urea permeability in vasopressin-treated IMCDs. Blockade of gene transcription did not reverse aldosterone-attenuated urea permeability. In conclusion, aldosterone directly regulates water reabsorption through a non-genomic mechanism. Aldosterone-attenuated water reabsorption may be related to decreased trafficking of AQP2 to the plasma membrane. There may be a sex difference apparent in the inhibitory effect of aldosterone on water reabsorption in the inner medullary collecting duct. This study is the first to show a direct effect of aldosterone to inhibit vasopressin-stimulated osmotic water permeability and urea permeability in perfused rat IMCDs.

Effects of hypertonicity on ADH-stimulated water permeability in rat inner medullary collecting duct

1990 ◽  
Vol 258 (2) ◽  
pp. F266-F272 ◽  
Author(s):  
S. P. Nadler
Keyword(s):  
Antidiuretic Hormone ◽  
Water Permeability ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Water Reabsorption ◽  
Cyclic Monophosphate ◽  
Collecting Ducts ◽  
Significant Augmentation ◽  
Medullary Collecting Duct ◽  
A Site

To assess the effects of increased tonicity on water reabsorption (Jv) in inner medullary collecting ducts (IMCD), antidiuretic hormone (ADH)-stimulated Jv and water permeability (PF) were determined in microperfused IMCD dissected from the inner medulla of rat kidney. In IMCD exposed to a 150-mosmol/kgH2O gradient in isotonic bath, ADH-stimulated PF averaged 719 +/- 93 microns/s. Symmetric addition of 75 mM NaCl to perfusate and bath resulted in a significant augmentation of ADH-stimulated PF (56%) that was reversible when initial solutions were restored. Despite the increase in PF, JV did not change but would have decreased by 16% (P less than 0.01) had PF not increased, because of the greater absolute axial increase in luminal tonicity that occurs with more hypertonic luminal solutions. When 150 mM mannitol was used to increase tonicity, similar effects were observed. However, 150 mM urea had no effect on ADH-stimulated PF. In IMCD exposed to 8-para-(chlorophenylthio)-adenosine 3',5'-cyclic monophosphate, addition of 75 mM NaCl to both and perfusate also resulted in a 76% increase in PF. These results are the first to demonstrate directly that increased effective tonicity augments ADH-stimulated PF in rat IMCD at a site distal to adenosine 3',5'-cyclic monophosphate generation. This effect may contribute to maintenance of medullary interstitial tonicity during antidiuresis by ensuring that most water reabsorption occurs more proximally within the IMCD.

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