Angiotensin-(1–7) in the basolateral amygdala attenuates the cardiovascular response evoked by acute emotional stress

• Evidence indicates that the heptapeptide Ang-(1–7) opposes Ang II actions.
• Brain Ang-(1–7) receptors plays a role in cardiovascular control.
• Ang-(1–7) attenuates the cardiovascular response to stress; site of action remains unknown.
• Basolateral amygdala is a key nucleus for responses to emotional stress.
• Ang-(1–7) in the amygdala attenuates cardiovascular response to emotional stress.

The basolateral amygdala (BLA) plays a critical role in mediating physiological responses to emotional stress. Recent data suggest that angiotensin-(1–7) [Ang-(1–7)] can act centrally attenuating the cardiovascular response to acute stress. We investigated whether Ang-(1–7) in the BLA plays a role in the cardiovascular response to emotional stress. Under anesthesia, guide cannulas were implanted into the BLA of Wistar rats. Five days later, the femoral artery was cannulated for mean arterial pressure (MAP) and heart rate (HR) recordings. Microinjections of Ang-(1–7) (5 or 50 pmol), the Mas receptor antagonist A-779 (100 pmol), Ang-(1–7)+A-779 (50+100 pmol, respectively), or vehicle (NaCl 0.9%, control) were performed after 24 h and rats were then submitted to stress trials. Injection of Ang-(1–7) into the BLA blocked the tachycardia (ΔHR: vehicle 135±23 vs. Ang-(1–7) 9±12 bpm; P<0.05) and the pressor response (ΔMAP: vehicle 28±3 mmHg vs. Ang-(1–7) 6±2 mmHg; P<0.05) produced by air jet stress. These effects were completely reversed by A-779 (ΔHR: 109±11 bpm; ΔMAP: 18±2 mmHg). Ang-(1–7) into the BLA also attenuated the pressor response evoked by cage-switch stress paradigm. These findings indicate that Ang-(1–7) can act in the BLA through the Mas receptors modulating the cardiovascular response evoked by emotional stress.