Objective    To observe the role of angiotensin Ⅱ (AngⅡ)- activated p38 MAPK and JNK in vascular protective responses following hemorrhagic shock in rats.     Methods    Eighty SD rats with hemorrhagic shock (40 males and 40 females)

weighing 200 to 230 g

were enrolled in this study. Effect of AngⅡ on the activity of p38 MAPK and JNK was observed in superior mesenteric artery (SMA) of rats after hemorrhagic shock. Effects of AngⅡ-activated p38 MAPK and JNK on vascular protective responses after hemorrhagic shock in rats were observed using the p38 MAPK and JNK antagonists (SB203580 and SP600125).     Results    The activity of p38 MAPK was increased after early hemorrhagic shock and then decreased after late hemorrhagic shock. The activity of p38 MAPK was 201.2% and 53.2% higher in rats with hemorrhagic shock than in normal controls at 0.5 h and 2 h after hemorrhagic shock

respectively (P0.01). The activity of JNK was increased with the prolongation of hemorrhagic shock

which was 308.8% higher in rats with hemorrhagic shock than in normal controls at 2 h after hemorrhagic shock (P0.01). AngⅡ-given at the late hemorrhagic shock could significantly increased the activity of p38 MAPK and JNK and the contractile response of SMA. SB203580 and SP600125 inhibited the AngⅡ-activated p38 MAPK and JNK activity

which was decreased to 52.9% and 44.8%

respectively (P0.05)

and suppressed the increased vascular reactivity due to AngⅡ-activated p38 MAPK and JNK

which was decreased to 60.5% and 65.0%

respectively (P0.01).     Conclusion    p38 MAPK and JNK are involved in the effect of AngⅡ on vascular protective responses following hemorrhagic shock in rats.