Key result
A low, non-hypertensive dose of Angiotensin II induced an early local and systemic inflammatory response, increasing TGF-β and IL-6 expression in cardiac arteries primarily via the AT1 receptor.
Why the study?
To verify if a low dose of angiotensin II can induce an inflammatory response in cardiac arteries even when blood pressure remains normal.
p-value: p=≤0.05
Low-dose Angiotensin II directly induces vascular inflammation in cardiac arteries via AT1 receptors, independent of its hypertensive effects.
Preclinical data warrant caution against clinical extrapolation; extends mechanistic evidence for AT1-mediated cardiac vascular inflammation but leaves human relevance open.
To verify if a low dose of angiotensin II (Ang II) can induce an inflammatory response in cardiac arteries, even though blood pressure remains at normal values. Were used C57Bl/6J male mice treated with a low dose of Ang II (30ng/kg IP) and AT1R blockers. Blood pressure was recorded after 10, 30, 60min, 2 and 6hours after Saline or Ang II injection. Time curve (30 and 60min, 2, 6, 12, 24, and 48hours after treatment) for expression of inflammatory markers was evaluated in cardiac arteries (TGF-β, IL-1β, IL-6, TNF-α and ICAM-1) by immunohistochemistry and western blot. Serum TNF-α and IL-6 were analyzed by ELISA. Although Ang II did not alter blood pressure, local TGF-α and IL-6 presented an early increase in cardiac arteries. IL-1β and ICAM-1 participated in a late response to Ang II (12 hours). Ang II group showed a systemic increase of IL-6 30 to 60 minutes after treatment. AT1 and AT2 receptor blockers (losartan, 20mg/kg, and PD123.319, 15mg/kg) were given alone or concomitant to Ang II. This combination showed that Ang II increases TGF-β and IL-6 by acting on the AT1 receptor in a fast response. IL-1β regulation by Ang II seems to be mediated by both AT1 and AT2 receptors. The results suggest that, independently of hemodynamic influences, Ang II, acting on AT1R, leads to the expression of inflammatory markers in cardiac vessels. AT2 receptor seems to be involved in the counterbalance of AT1R during modulation of IL-1β production in cardiac arteries.
No takes yet. Share an insight, caveat, or question.
Oliveira et al. (2023) studied Normotensive. Angiotensin II vs. Saline solution (NaCl 0.9%) was evaluated on Expression of inflammatory markers (TGF-β, IL-1β, IL-6, TNF-α, ICAM-1) in cardiac arteries (p=≤0.05). A low, non-hypertensive dose of Angiotensin II induced an early local and systemic inflammatory response, increasing TGF-β and IL-6 expression in cardiac arteries primarily via the AT1 receptor.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: