(Hypertension. 1997;30:704.)
© 1997 American Heart Association, Inc.
Articles |
From the Department of Physiology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil.
Correspondence to Oswaldo U. Lopes, MD, Departamento de Fisiologia, Universidade Federal de São Paulo, Escola Paulista de Medicina, Rua Botucatu, 862, CEP 04023-060, São Paulo, SP, Brazil. E-mail LopesU.Fisi{at}epm.br
Abstract The aim of the present study was to examine the
participation of NO in the rostral ventrolateral medulla (RVLM) of
freely moving rats. We utilized NO donors and L-arginine,
which were microinjected into the RVLM. Unilateral microinjection (100
nL) of 2.5 nmol sodium nitroprusside produced a biphasic response
consisting of an initial, rapid increase in arterial
pressure (AP) from 125±5 to 161±8 mm Hg (P<.01) and
a second, long-lasting response with a progressive increase in AP
(maximum
peak, 34±9 mm Hg; P<.01). Another NO
donor, S-nitroso-N-acetylpenicillamine (SNAP; 2.5
nmol), also produced immediate hypertension from 118±5
mm Hg to 168±7 mm Hg (P<.01) but without the
second, long-lasting response. L-Arginine (5, 24, and 140
nmol) produced a gradual increase in AP. L-Glutamate (5
nmol) microinjected into the RVLM produced an increase in AP from
122±9 mm Hg to 171±8 mm Hg (P<.01) and
bradycardia from 342±10 to 315±8 beats/min. This AP response was
significantly attenuated, from 115±7 to 128±9 mm Hg
(P<.05), after microinjection of methylene blue (3 nmol)
without alterations in heart rate. These results indicate
that NO may have an excitatory effect on the RVLM of freely moving
rats, probably in association with glutamatergic synapses via cGMP
mechanisms.
Key Words: amino acids blood pressure, arterial brain nitric oxide rostral ventrolateral medulla
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