Angiotensin‐(1–7) in the basolateral amygdala but not in the dorsomedial hypothalamus attenuates the cardiovascular response evoked by acute stress

Central administration of angiotensin‐(1–7) [Ang‐(1–7)] attenuates the cardiovascular response to stress, but the central targets remain to be determined. The dorsomedial hypothalamus (DMH) and basolateral amygdala (BLA) are critical sites for the physiological response to emotional stress. We investigated whether administration of Ang‐(1–7) into DMH and BLA change cardiovascular responses to acute stress. Under tribromoethanol anesthesia (250 mg/Kg i.p.) male Wistar rats (±330g) received guide cannula targeted to DMH or BLA (in separated groups). Four days later, femoral artery was cannulated for recording mean arterial pressure (MAP) or heart rate (HR). After 24h, microinjections into DMH and BLA were done before air jet stress (10L/min ‐ 10 min). In DMH experiments (3 groups, n=4–6) we injected Ang‐(1–7) [10 or 20 pmol/100nl] or vehicle [NaCl 0.9%, 100nl, control]. Into BLA (2 groups, n=5–6), microinjections were: Ang‐(1–7) [25pmol/200nl] or vehicle [200nl, control]. Compared to its respective control group, only microinjection of Ang‐(1–7) into BLA attenuated the increases in MAP (control ΔMAP: 29±2 vs. Ang 11±2mmHg, P<0.001) and heart rate (control ΔHR: 158±12 vs. Ang 82±14bpm; P<0.01) evoked by air stress. Our preliminary data indicates that the BLA, but not the DMH, may be a site where Ang‐(1–7) acts attenuating the cardiovascular response evoked by acute stress. Support: CNPq/FAPEMIG.