Salt sensitivity in response to renal injury requires renal angiotensin-converting enzyme

Recent evidence indicates that salt-sensitive hypertension can result from a subclinical injury that impairs the kidneys´ capacity to properly respond to a high-salt diet. However, how this occurs is not well understood. Here, we showed that although previously salt-resistant wild-type mice became s...

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Detalles Bibliográficos
Autores: Giani, Jorge Fernando, Bernstein, Kenneth E., Janjulia, Tea, Han, Jiyang, Toblli, Jorge Eduardo, Shen, Xiao Z., Rodriguez Iturbe, Bernardo, McDonough, Alicia A., Gonzalez Villalobos, Romer A.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2015
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/21485
Acceso en línea:http://hdl.handle.net/11336/21485
Access Level:acceso abierto
Palabra clave:Angiotensin-Converting Enzyme
Diet
Glomerular Filtration Rate
Hypertension
Inflammation
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Descripción
Sumario:Recent evidence indicates that salt-sensitive hypertension can result from a subclinical injury that impairs the kidneys´ capacity to properly respond to a high-salt diet. However, how this occurs is not well understood. Here, we showed that although previously salt-resistant wild-type mice became salt sensitive after the induction of renal injury with the nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester hydrochloride; mice lacking renal angiotensin-converting enzyme, exposed to the same insult, did not become hypertensive when faced with a sodium load. This is because the activity of renal angiotensin-converting enzyme plays a critical role in (1) augmenting the local pool of angiotensin II and (2) the establishment of the antinatriuretic state via modulation of glomerular filtration rate and sodium tubular transport. Thus, this study demonstrates that the presence of renal angiotensin-converting enzyme plays a pivotal role in the development of salt sensitivity in response to renal injury.