English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Aldosterone  is implicated in cardiac hypertrophy and fibrosis. We  tested the role of the mineralocorticoid receptor in a model of  angiotensin II–induced cardiac injury. We administered  spironolactone (SPIRO; 20 mg ·  kg−1 · d−1 ), valsartan (VAL; 10  mg · kg−1 ·  d−1 ), or vehicle to rats double transgenic  for the human renin and angiotensinogen genes (dTGR). We  investigated basic fibroblast growth factor (bFGF),  platelet-derived growth factor, transforming growth  factor-β1 , and the transcription factors AP-1  and nuclear factor (NF)-κB. We used immunohistochemistry,  electrophoretic mobility shift assays, and TaqMan RT-PCR. Untreated  dTGR developed hypertension, cardiac hypertrophy,  vasculopathy, and fibrosis with a 50% mortality rates at 7 weeks.  SPIRO and VAL prevented death and reversed cardiac  hypertrophy, while only VAL normalized blood pressure. Both  drugs prevented vasculopathy. bFGF was markedly upregulated in dTGR,  whereas platelet-derived growth factor-B and transforming growth  factor-β1 were little changed. VAL and SPIRO  suppressed this upregulation. Both AP-1 and NF-κB were  activated in dTGR compared with controls. VAL and SPIRO reduced  both transcription factors and reduced bFGF, collagen I, fibronectin,  and laminin in the interstitium. These findings show that  aldosterone promotes hypertrophy, cardiac  remodeling, and fibrosis, independent of blood pressure. The effects  involve AP-1, NF-κB, and bFGF. Mineralocorticoid receptor blockade  downregulates these effectors and reduces angiotensin  II–induced cardiac damage.

Mineralocorticoid Receptor Affects AP-1 and Nuclear Factor-κB Activation in Angiotensin II–Induced Cardiac Injury