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Skeletal Muscle Overexpression of SOD Normalizes the Exaggerated Exercise Pressor Reflex in Rats with Heart Failure
Author(s) -
Wang Hanjun,
Wang Weizhong,
Gao Lie,
Zucker Irving H.,
Wang Wei
Publication year - 2009
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.23.1_supplement.787.13
Subject(s) - medicine , endocrinology , reflex , heart failure , stimulation , contraction (grammar) , oxidative stress , skeletal muscle , chemistry
An sensitized exercise pressor reflex (EPR) in chronic heart failure (CHF), is believed to contribute to the exaggerated sympatho‐excitation observed during exercise in the CHF state. Accumulating evidence also shows that the exaggerated EPR in CHF may be due to an enhanced skeletal muscle mechanoreflex. However, the cause of the exaggerated EPR and the enhanced mechanoreflex in CHF are not well understood. Here, we hypothesized that muscle oxidative stress in CHF contributes to the exaggerated EPR and the enhanced mechanoreflex. We used the technique of adenoviral gene transfer to overexpress SOD proteins (AdSOD1 or AdSOD2, 1×10 12 particles in saline/ml, 50 μl, Adempty as a control) in the triceps surae muscle of CHF rats (2‐4 weeks). The EPR was induced by static contraction in response to electrical stimulation of the ventral roots (L4/L5) in decerebrate rats. The mechanoreflex was induced by passive stretch in decerebrate rats. Table 1 shows the effect of overexpression of SOD proteins on the EPR and mechanoreflex in CHF rats. These data indicate that muscle oxidative stress contributes to the exaggerated EPR and the enhanced mechanoreflex in CHF. 1 Effect of overexpression of SOD on the pressor response evoked by static contraction (EPR) or passive stretch in CHF rats.Values are Mean±SE, n=6 in each group,* P <0.05 vs Sham, ? P <0.05 vs CHF+Empty.