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University of Melbourne, Clinical Pharmacology and Therapeutics Unit, Austin and Repatriation Medical Centre, Heidelberg, Victoria 3084, Australia
Mechanisms underlying the depressor and
sympathoinhibitory responses evoked from the caudal medullary raphe
(MR) region were investigated in pentobarbital sodium-anesthetized,
paralyzed rats. Intermittent electrical stimulation (0.5 Hz, 0.5-ms
pulses, 200 µA) of the MR elicited a mixed sympathetic response that
consisted of a long-latency sympathoexcitatory (SE) peak (onset = 146 ± 7 ms) superimposed on an inhibitory phase (onset = 59 ± 10 ms). Chemical stimulation of the MR (glutamate;
Glu) most frequently elicited depressor responses accompanied by
inhibition of sympathetic nerve discharge. Occasionally, these
responses were preceded by transient pressor and SE responses. We
examined the influence of intermittent electrical stimulation (0.5 Hz,
0.5-ms pulses, 25-200 µA) and Glu stimulation of the MR on the
discharge of rostral ventrolateral medulla (RVLM) premotor SE neurons.
Peristimulus-time histograms of RVLM unit discharge featured a
prominent inhibitory phase in response to MR stimulation (onset = 20 ± 2 ms; duration = 42 ± 4 ms;
n = 12 units). Glu stimulation of the
MR reduced blood pressure (
37 ± 2 mmHg,
n = 19) and inhibited the discharge of
RVLM SE neurons (15 of 19 neurons). Depressor and
sympathoinhibitory responses elicited by chemical and electrical
stimulation of the MR region are mediated by inhibition of RVLM
premotor SE neurons and withdrawal of sympathetic vasomotor discharge.
blood pressure; sympathoinhibitory neurons
Deceased 12 May 1998. The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement"
in accordance with 18 U.S.C.
§1734 solely to indicate this fact.
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