Hostname: page-component-586b7cd67f-g8jcs Total loading time: 0 Render date: 2024-12-01T03:56:29.461Z Has data issue: false hasContentIssue false

Nature of ADH-Induced Endosomes In Toad Urinary Bladder Granular Epithelial Cells

Published online by Cambridge University Press:  02 July 2020

A.J. Mia
Affiliation:
Jarvis Christian College, Hawkins, Texas75765
L.X. Oakford
Affiliation:
UNTHSC at Fort Worth, Fort Worth, Texas76107.
A. Dibas
Affiliation:
UNTHSC at Fort Worth, Fort Worth, Texas76107.
T. Yorio
Affiliation:
UNTHSC at Fort Worth, Fort Worth, Texas76107.
Get access

Extract

Serosal ADH stimulation enhances water flow under an imposed osmotic gradient through insertion of water channels (aggrephores) into the mucosal plasma membrane of toad urinary bladder sacs. Following cessation of ADH actions, water channels are retrieved as endosomes that can be visualized by mucosal inclusion of horseradish peroxidase (HRP) into round vesicles, long tubules and multivesicular bodies within the cytosol (1,2,3). Endosomes also occur adjacent to golgi bodies or lysosomes (1,2,3). However, true nature of endosomes including their formation at the mucosal surface and their shuttling in granular cells is still unclear (4,5). Current studies were undertaken to understand the role of endosomes in water channel cycling in this renal membrane model.

Urinary bladder sacs removed surgically from doubly-pithed toads, were suspended at ends of glass tubes. Control (no hormone) and experimental bladder sacs were exposed to ADH for 10 min in the absence of osmotic gradient.

Type
Dynamics of Cellular Membrane Traffic
Copyright
Copyright © Microscopy Society of America

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.Masur, S. K. et al., Am. J. Physiol. (1984) 247 (Renal Fluid Electrolyte Physiol. 16): F370-F379.Google Scholar
2.Harris, W. H. et al., J. Clin. Invest. (1986) 78: 703712.CrossRefGoogle Scholar
3.Coleman, R. A. et al., J. Histochem. Cytochem. (1987) 35: 14051414.CrossRefGoogle Scholar
4.Ding, G. et al., Am. J. Physiol. (1988) 255 (Cell Physiol. 24):C641C652.CrossRefGoogle Scholar
5.Mia, A. J. et el., Mol. Biol. Cell (1997) 8: 207A.Google Scholar
6. Supported by grant: DAMD17-95-C-5086.Google Scholar