We recently reported an involvement of angiotensin II (ANG II) and the ANG II type 1 (AT₁) receptor in the hepatic expression of interleukin-1 (IL-1) induced in dehydrated rats by lipopolysaccharide (LPS). Here, we first confirmed that ANG II and AT₁-receptors contribute to the LPS-induced increase in the splenic concentration of IL-1 in dehydrated rats. We then aimed to investigate whether ANG II contributes to IL-1 production through a modulating effect on the activation of proinflammatory transcription factors (NF-B and AP-1) that is induced in the dehydrated rat's liver and spleen by intravenous injection of LPS. Surprisingly, LPS markedly increased the hepatic activation of NF-B, an effect that was significantly enhanced (rather than reduced) by pretreatment with an ANG-converting-enzyme (ACE) inhibitor or AT₁-receptor antagonist. Furthermore, the same ACE inhibitor and AT₁-receptor antagonist each increased the resting NF-B activity in the liver and spleen, although they had no effect on the LPS-induced splenic expression of NF-B. Both hepatic and splenic AP-1 expressions were enhanced by LPS. This response was significantly augmented by pretreatment with the AT₁-receptor antagonist (but not with the ACE inhibitor) in the spleen, while in the liver neither drug had any effect. These results suggest that the endogenous ANG II or AT₁-receptor suppresses the activation of hepatic or splenic transcription factors in dehydrated rats given LPS. Our results seem not to support the idea that NF-B and AP-1 play key roles in the ANG II-induced enhancement of the production of proinflammatory cytokines that is induced by LPS in dehydrated rats.