INVESTIGADORES
CHARA Osvaldo
artículos
Título:
Asymmetry in the osmotic response of a rat cortical collecting duct cell line: role of aquaporin-2.
Autor/es:
CHARA OSVALDO; FORD PAULA; RIVAROLA VALERIA; PARISI MARIO; CAPURRO CLAUDIA
Revista:
JOURNAL OF MEMBRANE BIOLOGY
Editorial:
Springer New York
Referencias:
Lugar: New York; Año: 2005 vol. 207 p. 143 - 150
ISSN:
0022-2631
Resumen:
Asymmetry in the osmotic response of a rat cortical collecting duct cell line: role of aquaporin-2.   Chara O, Ford P, Rivarola V, Parisi M, Capurro C.   Laboratorio de Biomembranas, Departamento de Fisiologia y Biofisica, Facultad de Medicina, Universidad de Buenos Aires, Argentina.   Transition from antidiuresis to diuresis exposes cortical collecting duct cells (CCD) to asymmetrical changes in environment osmolality, inducing an osmotic stress, which activates numerous membrane-associated events. The aim of the present work was to investigate, either in the presence or not of AQP2, the transepithelial osmotic water permeability (P(osm)) following cell exposure to asymmetrical hyper- or hypotonic gradients. For this purpose, transepithelial net volume fluxes were recorded every minute in two CCD cell lines: one not expressing AQPs (WT-RCCD(1)) and another stably transfected with AQP2 (AQP2-RCCD(1)). Our results demonstrated that the rate of osmosis produced by a given hypotonic shock depends on the gradient direction (osmotic rectification) only in the presence of apical AQP2. In contrast, hypertonic shocks elicit P(osm) rectification independently of AQP2 expression, and this phenomenon may be linked to modulation of basolateral membrane permeability. No asymmetry in transepithelial resistance was observed under hypo- or hypertonicity, indicating that rectification cannot be attributed to a shunt through the tight junction path. We conclude that osmotic rectification may be explained in terms of dynamical changes in membrane permeability probably due to activation/incorporation of AQPs or transporters to the plasma membrane via some mechanism triggered by osmolality.