REACTIVE OXYGEN SPECIES MODIFY REFLEX CARDIOVASCULAR-RESPONSES TO STATIC CONTRACTION

Reactive oxygen species can reflexly activate the cardiovascular syste m through stimulation of abdominal visceral afferents. The mechanism a ppears to involve hydroxyl radicals. We tested the hypothesis that rea ctive oxygen species contribute to the reflex cardiovascular response to static muscle contraction (i.e., the exercise presser reflex). Thus blood pressure and heart rate responses to 5 min of intermittent elec trically stimulated static contraction of the triceps surae muscles (1 5 s on, 15 s off) in anesthetized cats were compared before and after intravenous administration of the free radical scavengers dimethylthio urea (DMTU; 10 mg/kg; n = 8) or deferoxamine (nef; 10 mg/kg; it = 15). The contraction-induced presser response was augmented from 51 +/- 6 to 61 +/- 7 mmHg after treatment with DMTU (P < 0.05) and from 44 +/- 8 to 58 +/- 8 mmHg after administration of Def(P < 0.05). Correspondin g heart rate responses were not affected by either drug. Because this DMTU- or Def-induced augmentation of the exercise presser reflex may h ave been due to a reduction in free radical-evoked vasodilation in the contracting skeletal muscle, popliteal artery blood velocity was meas ured with a Doppler flow transducer before and during contraction in t he absence and presence of Def(n = 8). Blood velocity during contracti on was not altered by Def(16 +/- 5 vs. 24 +/- 6 cm/s). These data sugg est that reactive oxygen species exert an inhibitory effect on the exe rcise presser reflex that is not associated with their local vasodilat or properties. This response is opposite to that observed during stimu lation of visceral afferents by reactive oxygen species.