Markers of acute cardiovascular inflammation induced by angiotensin II in a murine model

Abstract

Angiotensin II has important physiological functions for the homeostasis of the cardiovascular system and may also induce to inflammatory responses. The aim of this study was to evaluate the effetc of subpressor angiotensin II (AngII) on expression of inflammatory markers in cardiac vessels. Were used C57Bl/6J male mice, treated with subpressor dose of AngII (30ng/kg IP), confirmed by carotid catheterization and arterial pressure measure after 10, 30, 60min, and 2 and 6hours of AngII injection (n=5/saline; n=5/AngII). Inflammatory markers were evaluated in cardiac vessels (TGF-beta, IL-6 and iNOS) by western blot, and localized in vessels by immunohistochemistry. Mice were evaluated after 1 and 24 hours to identify acute responses. Results were compared by ANOVA, using p≤0.05 as significant. Blood pressure measurements showed no changes in arterial pressure and heart rate. Protein analysis showed an increase of inflammatory markers in cardiac tissue after 1 hour TGF-beta (84%), IL-6 (90%) and iNOS (70%). However, these markers were unchanged after 24 hours. Immunohistochemistry analysis showed a specific increase in these markers associated to cardiac vessels. The results suggests that, independently on hemodynamic influences, Angiotensin II leads to expression of inflammatory markers in cardiac vessels in a short period, and this may represent a direct pro-inflammatory action mediated by angiotensin II.