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The attenuation of the stress evoked tachycardia produced by angiotensin‐(1–7) in the basolateral amygdala is reversed by blockade of Mas receptor
Author(s) -
Fontes Marco Antônio Peliky,
Figueiredo Muller Ribeiro Flávia Camargos,
Xavier Carlos Henrique,
Santos Robson Augusto Sousa,
Oscar Charles Gonzaga
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1091.25
Subject(s) - basolateral amygdala , angiotensin ii , endocrinology , medicine , saline , blockade , chemistry , receptor , anesthesia
We have previously reported that nanoinjection of angiotensin‐(1–7) [Ang‐(1–7)] into the basolateral amygdala (BLA) attenuates the cardiovascular response evoked by acute stress in rats. In this study we evaluated the contribution of Mas receptor in the anti‐stress effect produced by Ang‐(1–7) in the BLA. Under tribromoethanol anesthesia (250 mg/Kg i.p.), bilateral guide cannulas were implanted targeting the BLA of Wistar rats (n=5–6) for nanoinjection of saline (100 nl), Ang‐(1–7) (25 pmol/100 nl) or Ang‐(1–7) + A‐779 (25pmol+50pmol, 100 nl). Four days later, arterial lines were implanted for cardiovascular recordings. After 24h, nanoinjections into the BLA were performed followed by air jet stress (10L/min‐10min). In the saline group, stress evoked increases in MAP and HR (137±25 bpm; 24±2 mmHg). The attenuation of the tachycardia produced by Ang‐(1–7) was reversed by A‐779 [(Ang‐(1–7) −5±13 bpm vs. A‐779+Ang‐(1–7) 114±17 bpm, P<0.001]. The same was observed for the pressor response [Ang‐(1–7) 2±2 mmHg vs. A‐779+Ang‐(1–7) 15±1 mmHg, P<0.05]. We observed in two rats that the attenuation of the tachycardic response produced by 5 sessions of stress conditioning was reversed by injection of A‐779 into BLA. These findings indicate that the Ang‐(1–7) may reduce the cardiovascular response to acute stress in the amygdala acting via Mas receptor. Support: CAPES, FAPEMIG, CNPq.