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Interaction between angiotensin II (AngII) and brain‐derived neurotrophic factor (BDNF) in modulating K + currents
Author(s) -
Becker Bryan Keith,
Wang Hanjun,
Zucker Irving H.
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.lb834
Subject(s) - angiotensin ii , medicine , endocrinology , neurotrophic factors , brain derived neurotrophic factor , patch clamp , chemistry , electrophysiology , receptor
Sympathoexcitation in the setting of chronic heart failure and hypertension is a common and poor prognostic indicator during the progression of the disease. AngII has been widely implicated in the development of this pathology, however, the precise mechanisms by which AngII drives sympathoexcitation is incompletely understood. Recent evidence has emerged implicating the potential for an interaction between AngII and BDNF in the development of sympathoexcitation by increasing neuronal sensitivity. One likely mechanism leading to heightened neuronal sensitivity is the inhibition of outward K + currents. Here, we investigated the role AngII and BDNF have on modulating K + currents in CATH.a neuronal cell culture as measured by whole‐cell patch clamp. CATH.a neurons treated with exogenous BDNF (50ng/mL) for 2 hours exhibited decreased peak K + currents (21.5 ± 4.8 pA/pF, p<0.01 n=6) compared to control (63.3 ± 9.7 pA/pF, n=10). Acute superfusion of 50ng/mL BDNF for 10 minutes had no significant effect on K + currents. CATH.a treated for 6 hours with 100nM AngII exhibited decreased peak K + currents (70.3 ± 7.4 pA/pF, p<0.001 n=10) compared to control (136.7 ± 10.1 pA/pF, n=11). Cotreatment of AngII with anti‐BDNF antibody significantly attenuated this response (106.9 ± 11.9 pA/pF, p<0.05 n=7). These results indicate that BDNF may be a potential contributor to the decreased K + currents and increased neuronal sensitivity due to AngII and provide novel information about a potential role for BDNF in promoting sympathoexcitation.