Aquaporin 2 in the adenine-induced chronic kidney disease model

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Título

Aquaporin 2 in the adenine-induced chronic kidney disease model

Autor(es)

Albertoni Borghese, Maria Florencia; Majowicz, Mónica Patricia; Oronel, Lucas Humberto

Afiliación(es) del/de los autor(es)

Albertoni Borghese, Maria Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Majowicz, Mónica Patricia. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina
Oronel, Lucas Humberto. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas. Cátedra de Biología Celular y Molecular; Argentina

Resumen

Chronic kidney disease (CKD) is one of the leading health problems in the world. It is silent in the early stages and gradually progresses, inducing renal physiological and structural alterations. Moreover, CKD is associated with impaired life quality, increased risk for cardiovascular diseases, and reduced life expectancy. Different CKD animal models differ in underlying etiology, time of onset, and associated diseases. The 0.25% adenine diet induces progressive kidney damage, constituting an adequate model mimicking human CKD. Vasopressin (VP) was postulated as a mediator of CKD, mainly acting through its V2 receptors. However, the molecular mechanisms involved in the pathogenesis of this condition and its progression still are not entirely understood. This study aimed to evaluate if AQP2 expression is altered in an adenine-induced model of CKD in rats at early stages of development (two weeks) and to assess a potential beneficial effect of Tolvaptan (a V2 receptor antagonist) treatment. We showed an increased renal medullary AQP2 expression at two weeks of adenine administration. This increase was mainly cytoplasmic, explaining the increased urinary volume of CKD rats and suggesting a possible non-canonical role for AQP2. In addition, Tolvaptan effectively inhibited the V2 receptor in both control and CKD rats, decreasing AQP2 expression and increasing diuresis. Moreover, Tolvaptan slightly reduced BUN and plasma creatinine. On the other hand, the renal alterations induced by adenine in CKD rats were not prevented by Tolvaptan

Año de publicación

2024

Idioma

inglés

Formato (Tipo MIME)

application/vnd.openxmlformats-officedocument.spreadsheetml.sheet

Clasificación temática de acuerdo a la FORD

Ciencias de la salud

Condiciones de uso

Disponible en acceso abierto bajo licencia Creative Commons https://creativecommons.org/licenses/by/2.5/ar/

Repositorio digital

CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas

Identificador de proyecto

Consejo Nacional de Investigaciones Científicas y Técnicas/28720210100851CO