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Increased Rho‐kinase activity and reactive oxygen species contribute to the enhanced vasoconstrictor effects of angiotensin II in aortic rings from sepsis‐surviving rats (1158.3)

We hypothesized that changes in vascular reactivity contribute to the high mortality rate among patients discharged after severe sepsis/septic shock. Male Wistar rats were subjected to cecal ligation and puncture to induce sepsis (mortality around 30%) and aortic rings from survived animals were tested at 30 or 60 days after (S30 and S60 groups). The effects of KCl, phenylephrine, angiotensin I, CaCl2, acetylcholine and sodium nitroprusside did not change, but angiotensin II (AII)‐induced constriction was increased by 80% in aortic rings from S60. The removal of endothelium, incubation with L‐NAME (inhibitor of nitric oxide synthase), or inhibition of Rho‐kinase by Y‐27632 did not change the effects of AII in these vessels, which showed increased protein levels of both RhoA and ROCK II. Incubation with apocynin (NADPH oxidase inhibitor), SOD, or tempol (O2‐ scavenger) did not change the effect of AII in control rings, but avoided the increased reactivity to AII in vessels from S60 rats. The endogenous activity of SOD was decreased by 45 ± 3%, while the generation of LOOH and GSH were increased by 41 ± 12% and 98 ± 3.9% in the aorta of S60 rats. A selective fluorescent probe revealed an increased ROS generation (up to 30%) in vessels from S60 rats after stimulation with AII. In conclusion, aortic rings from sepsis‐surviving rats display increased reactivity to AII, which involves augmented activity of ROCK and oxidative stress.