Angiotensin II Increases HMGB1 Expression in the Myocardium Through AT1 and AT2 Receptors When Under Pressure Overload

High-mobility group box 1 (HMGB1) is increased in the myocardium under pressure overload (PO) and involved PO-induced cardiac remodeling. The mechanisms of upregulation HMGB1 expression have not been fully elucidated. In present study, a mouse transverse aortic constriction (TAC) model was used, an angiotensin II (Ang II) type (AT1) receptor inhibitor (losartan) or Ang 2 (AT2) (PD123319) administrated to mice for 14 days. Cardiac myocytes were cultured treated with 5 minutes 48 hours conditionally blockage AT1 AT2 receptor. TAC-induced hypertrophy observed at days after operation, which partially reversed by losartan, but PD123319. Similarly, upregulated levels both serum induced TAC reduced losartan. Elevated protein levels, mRNA significantly decreased Furthermore, culture media following treatment vitro, positively associated duration treatment. II-induced vitro inhibited losartan These results suggest that PO, are derived from myocytes, may be via receptors. Additionally, amelioration reduction through