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Remodeling of the guinea pig intracardiac plexus following pressure overload‐induced cardiac hypertrophy
Author(s) -
Baran Caitlin N,
Southerland E. Marie,
Ardell Jeffery L,
Hardwick Jean C
Publication year - 2008
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.22.1_supplement.1230.5
Subject(s) - intracardiac injection , medicine , pressure overload , electrophysiology , constriction , endocrinology , nitric oxide , descending aorta , muscle hypertrophy , histamine , anatomy , aorta , chemistry , cardiology , cardiac hypertrophy
Chronic pressure overload (PO) of guinea pig hearts was induced by a banding of the descending dorsal aorta (10–15% constriction). Animals were allowed to recover for 2 months, at which point the heart and intracardiac nerve plexus were isolated for electrophysiological and immunohistochemical analysis. Sham surgeries, in which the aorta was surgically visualized but undisturbed, were run in parallel. PO animals showed a significant increase in the size of the heart and lungs as a percent of body weight versus sham surgeries. Intracellular voltage recordings from parasympathetic postganglionic neurons showed no change in resting membrane properties in the sham or PO tissues versus age‐matched controls. However, neurons from PO hearts showed a significant increase in the magnitude of the histamine‐induced increase in neuronal excitability (as determined by the frequency of action potentials produced with depolarizing stimuli) as compared to both controls and sham surgeries. PO hearts also showed a three‐fold increase in the number of neuronal nitric oxide (nNOS) immunoreactive neurons (PO 15.2 + 1.8% versus controls 5.4 + 2.9%, p<0.02). These results indicate that chronic pressure overload induces a differential remodeling of intrinsic cardiac cellular phenotypes and functional up‐regulation of local network excitability. Supported by HL71830 (JLA) and R15 HL060619‐02 (JCH).