Riluzole is a neuroprotective
agent that is currently tested
for the treatment of multiple system
atrophy (MSA). Riluzole may
influence afferent and efferent
parts ofthe baroreflex due to glutamate
antagonistic effects. The effect
of riluzole on the efferent part
may be unmasked in MSA patients
with dysfunction of afferent structures
ofthe baroreflex. We compared
the effect of a single dose of
200 mg riluzole with placebo in 10
patients with probable MSA.
Brachial blood pressure and heart
rate were recorded at baseline and
for 120 minutes every 5 minutes after
ingestion ofr iluzole. For determination
of spontaneous baroreflex
sensitivity, continuous finger
blood pressure and ECG were
recorded. Cardiac stroke volume
was monitored using impedance
cardiography. The change in blood
pressure over a two hour period
was significantly greater with
riluzole than with placebo
(5 ± 5/2 ± 3 mmHg with placebo,
16 ± 6/10 ± 2mmHg with riluzole,
p < 0.001 by ANOVA). Systemic vascular
resistance increased 32 ± 6%
with riluzole. Baroreflex sensitivity,
the high and low frequency components
of heart rate variability, and
the low frequency component of
systolic blood pressure variability
were not different between placebo
and riluzole treatment. We conclude
that in MSA patients, manipulation
of glutamatergic transmission
with riluzole elicits a
moderate pressor response. The response
is explained by a marked
increase in systemic vascular resistance.
We propose that decreased
inhibition ofef ferent sympathetic
neurons may contribute to the response.