Abstract
We have previously reported that fictive locomotion‐evoked sympathoexcitation in rats with heart failure was exaggerated and that this exaggeration was suppressed by Tempol, a superoxide dismutase mimetic, injected bilaterally into the rostral ventrolateral medulla (RVLM). It should be noted that Tempol also possess a property to open ATP‐sensitive and Ca2+‐activated K+ channels. In the present study, we tested if Tiron, which does not chemically relate to Tempol but has a similar superoxide scavenging activity, injected bilaterally into the RVLM of rats with heart failure would reduce fictive locomotion‐evoked sympathoexcitation. Heart failure was induced in rats by coronary artery ligation. Fictive locomotion was evoked in decerebrated and paralyzed rats by electrical stimulation of the mesencephalic locomotor region. In the rats with heart failure (N8, fractional shortening < 35%), Tiron mirrored the effect of Tempol; bilateral injection into the RVLM of Tiron (10 mM, 100 nl) significantly (P<0.05) reduced the renal sympathoexcitatory and pressor responses to fictive locomotion by 42% and 43%, respectively. The present data support the concept that oxidative stress in the medulla of heart failure plays a role in excessively amplifying central command‐mediated sympathoexcitation. Supported by Mitsui Life Social Welfare Foundation Research Grant (to S. Koba).
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