Effect of hypoosmotic shock on the volume of renal collecting duct epithelial cells of brattleboro rats with hereditarily defective vasopressin synthesis

• Published in: Doklady. Biochemistry and biophysics 2013-03, Vol.449 (1), p.102-104
• Main Authors: Baturina, G. S., Katkova, L. E., Ilyaskin, A. V., Solenov, E. I., Ivanova, L. N.
• Format: Article
• Language: English
• Subjects: Animals; Biochemistry; Biological and Medical Physics; Biomedical and Life Sciences; Biophysics; Biophysics and Molecular Biology; Cell Size; Cells; Chemical synthesis; Epithelial Cells - cytology; Epithelial Cells - metabolism; Female; Fluoresceins - metabolism; Kidney diseases; Kidney Tubules, Collecting - cytology; Life Sciences; Male; Osmotic Pressure; Rats; Rodents; Vasopressins - biosynthesis; Vasopressins - deficiency
• ISSN: 1607-6729; 1608-3091
• DOI: 10.1134/S1607672913020130

The problem of maintaining a constant volume under conditions of extracellular and intracellular osmotic pressure fluctuations is particularly relevant for transport epithelium cells, such as renal collecting duct cells. The mechanisms regulating the cell volume in osmotic shock are specific for hypotensive and hypertensive effects [1, 2]. Recent studies have shown that the swelling rate of the cell in a hypoosmotic envi ronment and the effectiveness of regulatory volume decrease largely depend on the water permeability of the plasma membrane. The lipid bilayer of the cell membrane is highly permeable for water molecules due to the presence of specific proteins that form water channels (aquaporins, AQPs) [3]. Thus, the regulation of the water permeability of the cell membrane affects the parameters of the regulatory volume decrease (RVD). The transepithelial water permeability of renal collecting ducts increases as a result of AQP2 insertion into the apical membrane of cells in response to the neurohypophysial hormone vasopressin [4]. In the absence of the hormone or in the case of its inability to bind to receptors, the urine output and, respectively, the bodys fluid demands increase tenfold. In Brattle boro rats, derived from Long Evans rats [5], a single deletion in the vasopressin gene was found [6], which leads to disruption of the hormone synthesis [5, 7, 8]. Homozygous Brattleboro rats are characterized by a sharp decrease in the concentrating ability of the kid neys, polydipsia, and polyuria. In this study, we inves tigated the effect of the absence of endogenous vaso pressin in Brattleboro rats in response to changes in the volume of the principal cells of renal collecting ducts exposed hypoosmotic environment.