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Central administration of angiotensin‐(1‐7) markedly reduces the tachycardia evoked by acute psychological stress exposure
Author(s) -
Lima Augusto Martins,
Xavier Carlos Henrique,
Santos Robson Augusto Souza,
Fontes Marco Antônio Peliky
Publication year - 2009
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.23.1_supplement.609.5
Subject(s) - heart rate , medicine , femoral artery , anesthesia , angiotensin ii , ventricle , blood pressure , tachycardia , endocrinology
There is now extensive evidence that the activity of brain RAS is important in the control of anxiety‐related behaviors. In this study we investigated possible central effects of the heptapeptide angiotensin‐(1‐7) [Ang‐(1‐7)] in the cardiovascular reactivity to acute psychological stress. Under tribromoethanol anesthesia (250 mg/Kg i.p.) male wistar rats (?300g) received guide cannula into cerebral ventricle (i.c.v.) for microinjections of drugs. Four days later, a catheter was placed into femoral artery for recording cardiovascular parameters. After 24 h, three different doses of Ang‐(1‐7) [50, 100 and 200 pmol/2 ?l (n=5 each dose)] or vehicle [control, NaCl 0.9%, 2 ?l (n=6)] was administered i.c.v. and rats were submitted to air jet stress (10 L/min ‐ 10 min). In control experiments, the tachycardia evoked by air stress (? 148 ± 18 bpm) was markedly attenuated after 100 and 200 pmol i.c.v. injections of Ang‐(1‐7) (? 80 ± 18 bpm and ? 75 ± 29 bpm, p <0.05, respectively). This attenuation was observed throughout the 10 min stress trial. After treatment with these doses of Ang‐(1‐7), heart rate during the post‐stress recovery period was also lower than that seen after treatment with vehicle (vehicle 449 ± 25 bpm; Ang‐(1‐7) 100 pmol 382 ± 11 bpm; 200 pmol 377 ± 22 bpm; p <0.05) . Changes in blood pressure caused by air jet stress (21 ± 11 mmHg after vehicle) were more variable and not significantly altered by any dose of Ang‐(1‐7). We conclude that Ang‐(1‐7) might act in central regions attenuating the cardiac response evoked by acute psychological stress. Financial Support: CNPq, FAPEMIG, PRONEX.