Angiotensin II increases the expression of (pro)renin receptor during low-salt conditions

ALEXIS ANTONIO GONZALEZ PARRA, Joel P. Womack, Liu Liu, Dale M. Seth, Minolfa C. Prieto

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

17 Citas (Scopus)

Resumen

Background: Evidence indicates that chronic angiotensin II (AngII) infusion increases (pro)renin receptor ((P)RR) expression in renal inner medullary collecting duct (IMCD) cells. Recently, it has been shown that renal (P)RR expression is augmented during a low-salt (LS) diet. However, the role of AngII in mediating the stimulation of (P) RR during LS conditions is unknown. We hypothesized that AngII mediates the increased expression of (P)RR during low-salt conditions in IMCDs.

Methods: (P)RR expression and AngII levels were evaluated in Sprague-Dawley rats fed a LS diet (0.03% NaCl) and normal salt (NS; 0.4% NaCl) for 7 days. We examined the effects of sodium reduction (130 mM NaCl) and AngII on (P)RR expression in IMCDs isolated in hypertonic conditions (640 mOsmol/L with 280 mM NaCl).

Results: Plasma renin activity in LS rats was significantly higher than rats fed with NS (28.1 ± 2.2 versus 6.7 ± 1.1 ng AngI·mL-1·hr-1; P < 0.05), as well as renin content in renal cortex and medulla. The (P)RR mRNA and protein levels were higher in medullary tissues from LS rats but did not change in the cortex. Intrarenal AngII was augmented in LS compared with NS rats (cortex: 710 ± 113 versus 277 ± 86 fmol/g, P < 0.05; medulla: 2093 ± 125 versus 1426 ± 126 fmol/g, P < 0.05). In cultured IMCDs, (P)RR expression was increased in response to LS or AngII treatment and potentiated by both treatments (both at 640 mOsmol/L).

Conclusions: These data indicate that (P)RR is augmented in medullary collecting ducts in response to LS and that this effect is further enhanced by the increased intrarenal AngII content.

Idioma originalInglés
Páginas (desde-hasta)416-422
Número de páginas7
PublicaciónAmerican Journal of the Medical Sciences
Volumen348
N.º5
DOI
EstadoPublicada - 1 ene 2014

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