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Department of Physiology, University of South Alabama College of Medicine, Mobile, Alabama 36688
In this
study, we tested the hypothesis that nitric oxide (NO) production in
the dorsal horn is involved in producing the pressor reflex elicited by
static contraction of skeletal muscle. Cats were anesthetized with
-chloralose (80 mg/kg) and urethane (100 mg/kg), and a laminectomy
was performed. With the exception of the
L7 dorsal root, the dorsal and
ventral roots from L5 to S2 were sectioned on one side and
static contraction of the ipsilateral triceps surae muscle was evoked
by electrically stimulating the peripheral ends of the
L7 and
S1 ventral roots. Dialysis of the NO synthase inhibitor
NG-nitro-L-arginine
methyl ester (L-NAME; 50 mmol/l
syringe concentration, based upon dose-response data) into the dorsal
horn at L6 and S1 failed to attenuate the peak
change in mean arterial pressure (MAP) evoked by static contraction
(
MAP in mmHg: 57 ± 5 before and 50 ± 6 after 2 h of L-NAME). However, this
dialysis of L-NAME reduced the
magnitude of the initial pressor response as the MAP at 10 s of the contraction fell from 27 ± 4 to 17 ± 4 mmHg. On the
other hand, 2 h of L-arginine
dialysis (50 mmol/l) shifted the curve representing the time course of
the pressor response upward and increased the peak pressor response to
static contraction from 51 ± 9 to 68 ± 9 mmHg. A 2-h dialysis
of D-NAME (50 mmol/l), the
inactive enantiomer of L-NAME,
had no effect on the time course or the peak pressor response (MAP
in mmHg: 78 ± 12 before and 72 ± 15 after). These data suggest
that NO production in the dorsal horn has a modulatory influence on the
pressor reflex evoked by static contraction of skeletal muscle and that
increasing the level of NO in the dorsal horn enhances the excitability
of dorsal horn cells to muscle afferent input.
cats; exercise pressor reflex; excitatory amino acids; spinal cord; muscle afferent neurons; blood pressure
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