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- Title
Aldosterone Does Not Contribute to Renal p21 Expression During the Development of Angiotensin II-Induced Hypertension in Mice.
- Authors
Nakano, Daisuke; Lei, Bai; Kitada, Kento; Hitomi, Hirofumi; Kobori, Hiroyuki; Mori, Hirohito; Deguchi, Kazushi; Masaki, Tsutomu; Minamino, Tohru; Nishiyama, Akira
- Abstract
BackgroundWe recently reported that aldosterone-induced cellular senescence via an increase in p21, a cyclin-dependent kinase (CDK) inhibitor, in rat kidney and cultured human proximal tubular cells. In the present study, we investigated the contribution of aldosterone to the renal p21 expression and senescence during the development of angiotensin II (AngII)-induced hypertension.MethodsMice received 1% salt in drinking water and vehicle or AngII, and were divided into five groups: 1, vehicle; 2, AngII; 3, AngII+olmesartan; 4, AngII+eplerenone; and 5, AngII+hydralazine.ResultsPlasma aldosterone levels were increased by AngII infusion. Eplerenone further elevated the plasma aldosterone level, but olmesartan and hydralazine did not. AngII group showed significant increase in blood pressure compared to vehicle. Olmesartan and hydralazine, but not eplerenone, suppressed the AngII-salt hypertension. The increase in urinary protein excretion by AngII-salt was suppressed only by olmesartan. AngII with high salt induced a greater expression of p21 mRNA in the kidney than vehicle. Olmesartan abolished the increase in p21 expression, whereas neither eplerenone nor hydralazine affected it. AngII with high salt did not change the expression of p16, another CDK inhibitor. The mice lacking p21 showed identical changes on blood pressure and albuminuria in response to AngII with high salt compared to wild type.ConclusionThese results suggest that aldosterone does not predominantly contribute to renal p21 expression and senescence during the development of AngII-salt hypertension, and that the increase in p21 in the kidney is not likely involved in the development of hypertension and albuminuria.American Journal of Hypertension (2012); doi:10.1038/ajh.2011.224
- Subjects
CYCLIN-dependent kinases; LABORATORY rats; ANGIOTENSIN II; ALDOSTERONE; MESSENGER RNA; CHRONIC kidney failure; HYDRALAZINE; GENE expression
- Publication
American Journal of Hypertension, 2012, Vol 25, Issue 3, p354
- ISSN
0895-7061
- Publication type
Article
- DOI
10.1038/ajh.2011.224