Key result
Angiotensin-(1-7) ICV infusion in hypertensive rats decreased TNF-α levels, increased IL-10, and reduced ACE activity and AT1 receptor gene expression.
Why the study?
Putative central mechanisms mediating the antihypertensive effects of chronic intracerebroventricular Ang-(1-7) infusion, including inflammatory mediators, RAS components, and hypothalamic proteomic changes, remained to be investigated.
Does ICV infusion of Ang-(1-7) modulate central inflammatory mediators and RAS components in hypertensive rats?
Does ICV infusion of Ang-(1-7) modulate central inflammatory mediators and RAS components in hypertensive rats?
Central administration of Ang-(1-7) in hypertensive rats promotes anti-inflammatory effects and modulates the renin-angiotensin system in the hypothalamus.
Hypothesis-generating for central RAS modulation in hypertension models; leaves open human CNS-targeted translation.
Previous data showed hypertensive rats subjected to chronic intracerebroventricular (ICV) infusion of angiotensin-(1-7) presented attenuation of arterial hypertension, improvement of baroreflex sensitivity, restoration of cardiac autonomic balance and a shift of cardiac renin-angiotensin system (RAS) balance toward Ang-(1-7)/Mas receptor. In the present study, we investigated putative central mechanisms related to the antihypertensive effect induced by ICV Ang-(1-7), including inflammatory mediators and the expression/activity of the RAS components in hypertensive rats. Furthermore, we performed a proteomic analysis to evaluate differentially regulated proteins in the hypothalamus of these animals. For this, Sprague Dawley (SD) and transgenic (mRen2)27 hypertensive rats (TG) were subjected to 14 days of ICV infusion with Ang-(1-7) (200 ng/h) or 0.9% sterile saline (0.5 μl/h) through osmotic mini-pumps. We observed that Ang-(1-7) treatment modulated inflammatory cytokines by decreasing TNF-α levels while increasing the anti-inflammatory IL-10. Moreover, we showed a reduction in ACE activity and gene expression of AT1 receptor and iNOS. Finally, our proteomic evaluation suggested an anti-inflammatory mechanism of Ang-(1-7) toward the ROS modulators Uchl1 and Prdx1.
No takes yet. Share an insight, caveat, or question.
Kangussu et al. (2021) studied Hypertension. Angiotensin-(1-7) vs. 0.9% sterile saline (0.5 μl/h) was evaluated on Inflammatory mediators and the expression/activity of the RAS components. Angiotensin-(1-7) ICV infusion in hypertensive rats decreased TNF-α levels, increased IL-10, and reduced ACE activity and AT1 receptor gene expression.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: