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Elevated brain‐derived neurotrophic factor (BDNF) levels in the paraventricular nucleus (PVN) increase blood pressure, heart rate and indices of sympathetic activity
Author(s) -
Erdos Benedek,
Backes Iara,
McCowen Michael L,
Scheuer Deborah A
Publication year - 2013
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.27.1_supplement.1118.12
Subject(s) - medicine , endocrinology , heart rate , blood pressure , brain derived neurotrophic factor , neurotrophic factors , heart rate variability , chemistry , receptor
BDNF expression increases in the PVN during stress, but its role in mediating stress‐induced rises in blood pressure (BP) and heart rate (HR) is unclear. We tested the hypothesis that overexpression of BDNF within the PVN would elevate baseline BP and HR and would augment BP and HR responses to stress. BP was recorded in male Sprague‐Dawley rats using telemetry. At 11wks of age, adeno‐associated viral vectors [AAV2‐GFP (n=8) or AAV2‐BDNF (n=9)] were injected bilaterally into the PVN. BP recording continued for 4 wks, and responses to a 15 min water stress (WS, 1cm deep, 25 °C) and to a 60 min restraint stress (RS) were evaluated during wks 3 and 4. BDNF overexpression significantly increased BP and HR. At the end of week 4, daytime BP was 99±2 (GFP) and 122±3 mmHg (BDNF, p<0.01), while daytime HR was 314±4 (GFP) and 394±9 bpm (BDNF, p<0.01). BDNF treatment also significantly (p<0.05) increased sympathetic tone as indicated by HR variability (LF/HF ratio was 0.32±0.05 in GFP, 0.86±0.20 in BDNF rats) and BP variability (LF power was 1.6±0.1 mmHg 2 in GFP, 5.0±1.2 mmHg 2 in BDNF rats). However, BP and HR increases to WS and RS were significantly (p<0.05) reduced in BDNF (e.g. 25±1 and 28±2 mmHg) compared to GFP rats (33±3 and 36±2 mmHg). We conclude that BDNF is an important regulator of BP, HR and sympathetic tone in the PVN, but may not augment stress‐induced BP and HR responses. Supported by AHA 11SDG7560022, an AFAR research grant, and by NIH #HL76807, #HL93186.