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Activation of Central Angiotensin Type 2 Receptors by Compound 21 Suppresses Sympathetic Outflow in Rats with Chronic Heart Failure
Author(s) -
Gao Juan,
Xiao Liang,
Chao Jie,
Zucker Irving H.,
Gao Lie
Publication year - 2011
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.25.1_supplement.651.11
In previous studies, we demonstrated that, in normal rats, intracerebroventricular (icv) infusion of Compound 21 (C21), a nonpeptide AT2R agonist, decreased arterial blood pressure (BP) and norepinephrine (NE) excretion. In this experiment, we determined the effects of central treatment of C21 on sympathetic drive in rats with coronary ligation induced chronic heart failure (CHF). C21 was icv infused by a Micro‐osmotic pump at a rate of 0.5μg/μl/2hrs for 7 days. During this time, BP and heart rate were continually recorded by radio telemetry to analyze arterial baroreflex function (ABR) in the conscious state. On day 7 of treatment, the rats were anesthetized and renal sympathetic nerve activity (RSNA) was directly recorded to determine baseline sympathetic tone. We found that: (1) C21 treated CHF rats exhibited a higher ABR gain than control CHF rats from day 4 until day 7 of the treatment (3.1 ± 0.15 vs 2.3 ± 0.47 at day 4; 3.1 ± 0.40 vs 2.3 ± 0.16 at day 5; 3.0 ± 0.35 vs 1.9 ± 0.41 at day 6; 2.7 ± 0.30 vs 2.0 ± 0.43 at day 7; bpm/mmHg, P < 0.05), but no significant effect was found in normal rats; (2) Under anesthesia, the baseline RSNA was significantly lower in C21 treated CHF rats than that in control CHF rats at day 7 after treatment (26.7 ± 0.1 % of Max vs 39.1 ± 0.6 % of Max, P < 0.05). These results suggest that, in CHF rats, activation of central AT2R by C21 evoked a sympatho‐inhibition via improvement of arterial baroreflex function.