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Heart Rate Variability and Central Angiotensin II Receptors in Heart Failure: Role of Exercise Training
Author(s) -
Mousa Tarek M,
Cornish Kurtis G,
Zucker Irving H
Publication year - 2006
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.20.4.a393-b
Subject(s) - heart rate variability , angiotensin ii receptor type 1 , medicine , angiotensin ii , heart failure , cardiology , endocrinology , renin–angiotensin system , heart rate , receptor , blood pressure
Nebraska Medical Center, Omaha, Nebraska, 68198‐5850 Exercise training (EX) has become an important modality enhancing survival of patients with chronic heart failure (CHF). Heart rate variability (HRV) is a non‐invasive method assessing sympathovagal balance and predicting mortality in CHF. Enhanced HRV occurs in CHF following EX. We showed a down‐regulation of brain angiotensin II receptors (AT 1 ), a reduction in plasma Ang II and normalization of baseline renal sympathetic nerve activity (SNA) and an enhanced HRV for total power and standard deviation of R‐R interval (SDRR) with EX in a rapid pacing model of CHF in New Zealand white rabbits. We hypothesized that prevention of Ang II normalization in CHF‐EX rabbits would prevent the beneficial effects of EX on AT 1 expression, SNA and HRV. The table shows HRV parameters, baseline SNA and AT 1 expression using Western‐blot and RT‐PCR in the rostral portion of the ventrolateral medulla. When plasma Ang II levels were “clamped” and prevented from normalization with EX, down‐regulation of AT 1 expression was abolished and the total power was depressed through a reduction in the low frequency (LF) component of the total power (TP). The enhanced SDRR with EX was preserved despite Ang II infusion with EX. These data suggest that the reduction in plasma Ang II and/or AT 1 expression may be responsible for lowering SNA and that Ang II influences on HRV are reflected by the LF component of the TP and this influence does not affect SDRR, perhaps due to maintenance of vagal tone following EX in CHF. NIH grant PO‐I HL‐62222