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Peripheral activation of ACE2‐Ang‐(1–7)‐Mas axis reduces the cardiovascular reactivity to acute stress in rats
Author(s) -
Lima Augusto Martins,
Xavier Carlos Henrique,
Santos Robson Augusto Souza,
Raizada Mohan K.,
Ferreira Anderson J.,
Fontes Marco Antônio Peliky
Publication year - 2010
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.24.1_supplement.625.6
Subject(s) - bradycardia , heart rate , medicine , tachycardia , endocrinology , blood pressure , peripheral , femoral artery , endogeny , anesthesia , chemistry
We recently reported that central activation of ACE2‐Ang‐(1–7)‐Mas axis markedly reduces stress‐induced tachycardia. In the present study we investigated the peripheral contribution of ACE2‐Ang‐(1–7) axis on the cardiovascular reactivity to acute stress exposure. Under tribromoethanol anesthesia, male Wistar rats (300g) received cannulas into femoral artery and vein for recording cardiovascular parameters and drugs injection, respectively. After 24h, Ang‐(1–7) [2.5nmol/Kg (n=8)], XNT, an activator of endogenous ACE2 [1μmol/Kg (n=6)] or saline [NaCl 0.9% (n=8)] were intravenously (i.v.) injected immediately before starting air jet stress (10 l/min‐10 min). Tachycardia evoked by air stress (Δ136±22 bpm) was greatly attenuated ( P <0.05) by i.v. injections of Ang‐(1–7) (Δ61± 25 bpm), while XNT treatment changed the HR response to a bradycardia (Δ−44±7 bpm). These effects were observed throughout 10min stress trial. Heart rate during the post‐stress recovery period was also lower ( P <0.05) in the groups treated with Ang‐(1–7) (412±20 bpm) and XNT (306±12 bpm), compared to vehicle (482±23 bpm). Changes ( P <0.05) in blood pressure caused by air jet stress (Δ18±4 mmHg) were abolished by XNT (Δ−8±11 mmHg) and attenuated by Ang‐(1–7) (Δ9±3 mmHg). These current data extend our recent findings indicating that activation of ACE2‐Ang‐(1–7)‐Mas axis attenuates the cardiovascular reactivity to acute stress. Support CNPq and Fapemig.