Artículo
Angiotensin II mediates Tyr-dephosphorylation in rat fetal kidney membranes
Fecha de publicación:
12/2003
Editorial:
Springer
Revista:
Molecular and Cellular Biochemistry
ISSN:
0300-8177
e-ISSN:
1573-4919
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
Angiotensin II (Ang II) elicits a variety of physiological effects through specific Ang II receptors in numerous tissues. In addition, Ang II is a modulator of cellular growth and exerts a positive or negative effect on cell growth depending on which receptor subtype is activated. Expression of the intrarenal AT2 receptors occurs at its highest levels in the fetal kidney, with a rapid decline after birth. In the present paper, we performed a study on the signaling mechanism of Ang II receptors in rat fetal (E20) kidney, a rich source of AT2 receptors, where both Ang II receptor subtypes are present. Ang II induces Tyr-dephosphorylation of proteins in rat fetal kidney membranes. The response is dose-dependent, with a reduction of 20% with respect to the control (100%), signal that is completely reversed by Ang II AT2 competitor PD123319. Orthovanadate, the inhibitor of phospho-Tyr-phosphatases (PTPase), reverts Ang II effect, suggesting the involvement of a protein tyrosine phosphatase. The peptide analog of Ang II, CGP42112, exhibits an agonist effect, which is dose-dependent. Thus, in rat fetal (E20) kidney, the Ang-induced protein Tyr-dephosphorylation of several proteins is mediated by AT2 receptors, mechanism that involves an orthovanadate senitive PTPase.
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Articulos(IMIBIO-SL)
Articulos de INST. MULTIDICIPLINARIO DE INV. BIO. DE SAN LUIS
Articulos de INST. MULTIDICIPLINARIO DE INV. BIO. DE SAN LUIS
Citación
Alvarez, Sergio Eduardo; Fuentes, Lucia Beatriz; Ciuffo, Gladys Maria; Angiotensin II mediates Tyr-dephosphorylation in rat fetal kidney membranes; Springer; Molecular and Cellular Biochemistry; 254; 1-2; 12-2003; 137-143
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