Central Administration of Angiotensin-(1-7) Improves Vasopressin Impairment and Hypotensive Response in Experimental Endotoxemia

Figures

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  Figure 1. Central administration of Ang-(1-7) did not attenuate neuroinflammation in endotoxemia. Effect of central Ang-(1-7) on the TNF (A,D), NOS2 (B,E), and IL10 (C,F) gene expression in PVN and SON of rats 6 h after LPS administration (1.5 mg/Kg, i.v.). Ang-(1-7) (0.3 nmol in 2 µL, i.c.v.) was injected 1 min before LPS. Data are expressed as the mean ± SEM, n = 7–9. ANOVA, followed by Bonferroni post-hoc test. * p < 0.05 versus Saline (i.c.v.) + Saline (i.v.) group.

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  Figure 2. Central administration of Ang-(1-7) attenuated systemic inflammation in endotoxemic rats via Mas receptor. Effect of central Ang-(1-7) on the TNF-α (A), IL-1β (B), IL-6 (C), IL-10 (D), NOx (E), and TBARS (F) levels in rats 6 h after LPS administration (1.5 mg/Kg, i.v.). A779 (3 nmol in 2 µL, i.c.v.), a selective antagonist for Mas receptor, was injected 30 min before Ang-(1-7) administration (0.3 nmol in 2 µL, i.c.v.). Data are expressed as the mean ± SEM, n = 7–12. ANOVA, followed by Bonferroni post-hoc test. * p < 0.05 versus Saline (i.c.v.) + Saline (i.v.) group, # p < 0.05 versus Saline (i.c.v) + LPS (i.v.) group, and & p < 0.05 versus Ang-(1-7) (i.c.v) + LPS (i.v.) group.

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  Figure 3. Central administration of Ang-(1-7) increased AVP gene expression in endotoxemic rats. Effect of central Ang-(1-7) on the AVP (A,C) and CRH (B,D) gene expression in PVN and SON of rats 6 h after LPS administration (1.5 mg/Kg, i.v.). Ang-(1-7) (0.3 nmol in 2 µL, i.c.v.) was injected 1 min before LPS. Data are expressed as the mean ± SEM, n = 7-9. ANOVA, followed by Bonferroni post-hoc test. * p < 0.05 versus Saline (i.c.v.) + Saline (i.v.) group, # p < 0.05 versus Saline (i.c.v) + LPS (i.v.) group.

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  Figure 4. Central administration of Ang-(1-7) restored plasma AVP levels in endotoxemic rats via Mas receptor. Effect of central Ang-(1-7) on the AVP (A) and corticosterone (B) plasma levels in rats 6 h after LPS administration (1.5 mg/Kg, i.v.). A779 (3 nmol in 2 µL, i.c.v.), a selective antagonist for Mas receptor, was injected 30 min before central Ang-(1-7) administration (0.3 nmol in 2 µL, i.c.v.). Data are expressed as the mean ± SEM, n = 7–10. ANOVA, followed by Bonferroni post-hoc test. * p < 0.05 versus Saline (i.c.v.) + Saline (i.v.) group, # p < 0.05 versus Saline (i.c.v) + LPS (i.v.) group, and & p < 0.05 versus Ang-(1-7) (i.c.v) + LPS (i.v.) group.

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  Figure 5. Central Ang-(1-7) restored vascular hyporesponsiveness in endotoxemic rats. Effect of central Ang-(1-7) (0.3 nmol in 2 µL, i.c.v.) in vascular reactivity of the thoracic aorta to NE in the absence (A) or presence of aminoguanidine, a NOS2 selective inhibitor (100 μmol/L) (B), and AVP (1 nmol/L) (C) in rats 6 h after LPS administration (1.5 mg/Kg, i.v.). Data are expressed as the mean ± SEM, n = 5–7. ANOVA, followed by Bonferroni post-hoc test. * p < 0.05 versus Saline (i.c.v.) + Saline (i.v.) group and # p < 0.05 versus Saline (i.c.v) + LPS (i.v.) group.

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  Figure 6. Central Ang-(1-7) prevented LPS-induced hypotension in endotoxemic rats. Effect of central Ang-(1-7) (0.3 nmol in 2 µL, i.c.v.) on mean arterial blood pressure (MABP) (A) and heart rate (HR) (B) in rats submitted to endotoxemia (LPS, 1.5 mg/Kg, i.v.) for a 6-h period. Data are expressed as the mean ± SEM, n = 6–9. ANOVA, followed by Bonferroni post-hoc test. * p < 0.05 versus Saline (i.c.v.) + Saline (i.v.) group, and # p < 0.05 versus Saline (i.c.v) + LPS (i.v.) group.