About this item:

72 Views | 36 Downloads

Author Notes:

jeff.sands@emory.edu; Tel.: +1-404-7272-525; Fax: +1-404-7273-425

Conceptualization, J.M.S.; Data curation, F.M., E.L.R. and J.D.K.; Funding acquisition, J.M.S.; Investigation, Y.W.; Project administration, J.M.S.; Writing—original draft, Y.W.; Writing—review & editing, J.D.K. and J.M.S. All authors have read and agreed to the published version of the manuscript.

The authors declare no conflict of interest with the representation or interpretation of the reported research results.

Subjects:

Research Funding:

This work was supported by NIH grant R01-DK41707 and AHA Career Development Grant #18CDA34060053.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell Biology
  • mineralocorticoid receptor
  • natriuresis
  • non-genomic
  • AQP2
  • urea transport
  • UT-A1 UREA TRANSPORTER
  • AQP2 EXPRESSION
  • PHOSPHORYLATION
  • PERMEABILITY
  • MECHANISMS
  • RECEPTOR
  • TRANSCRIPTION
  • ACCUMULATION
  • TRAFFICKING
  • INHIBITION

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

Tools:

Journal Title:

CELLS

Volume:

Volume 9, Number 4

Publisher:

Type of Work:

Article | Final Publisher PDF

Abstract:

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.

Copyright information:

© 2020 by the authors.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
Export to EndNote