Reactive oxygen species modify the reflex cardiovascular response
to static contraction.
Bonigut, Stefanie, Charles L. Stebbins, and John C. Longhurst.
Department of Internal Medicine, Division of Cardiovascular
Medicine and Department of Human Physiology, University of
California, Davis, California 95616
APStracts 3:0207A, 1996.
Reactive oxygen species can reflexly activate the cardiovascular
system through stimulation of abdominal visceral afferents. The
mechanism appears to involve hydroxyl radicals. We tested the
hypothesis that reactive oxygen species contribute to the reflex
cardiovascular response to static muscle contraction (i.e. the
exercise pressor reflex). Thus, blood pressure and heart rate
responses to 5 min of intermittent electrically-stimulated static
contraction of the triceps surae muscles (15 s on, 15 s off) in
anesthetized cats were compared before and after intravenous
administration of the free radical scavengers dimethylthiourea (DMTU,
10 mg/kg; n=8) or deferoxamine (DEF, 10 mg/kg; n=15). The
contraction-induced pressor response was augmented from 51+/-6 mmHg
to 61+/-7 mmHg after treatment with DMTU (P<0.05) and from 44+/
-8 mmHg to 58+/-8 mmHg following administration of DEF (P<0.05).
Corresponding heart rate responses were not affected by either drug.
Since this DMTU- or DEF-induced augmentation of the exercise pressor
reflex may have been due to a reduction in free radical evoked
vasodilation in the contracting skeletal muscle, popliteal artery
blood velocity was measured with a doppler flow transducer before and
during contraction in the absence and presence of DEF (n=8). Active
blood velocity was not altered by DEF (16+/-5 cm/s vs. 24+/-6 cm/s).
These data suggest that reactive oxygen species exert an inhibitory
effect on the exercise pressor reflex that is not associated with
their local vasodilator properties. This response is opposite that
observed during stimulation of visceral afferents by reactive oxygen
species.
Received 23 October 1995; accepted in final form 9 April 1996.
APS Manuscript Number A1141-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96