An overview of the role of ventrolateral medulla (VLM) in regulation of car
diovascular activity is presented. A summary of VLM anatomy and its functio
nal relation to other areas in the central nervous system is described. Ove
r the past few years, various studies have investigated the VLM and its inv
olvement in cardiovascular regulation during static muscle contraction, a t
ype of static exercise as seen, for example, during knee extension or hand-
grip exercise. Understanding the neural mechanisms that are responsible for
regulation of cardiovascular activity during static muscle contraction is
of particular interest since it helps understand circulatory adjustments in
response to an increase in physical activity. This review surveys the role
of several receptors and neurotransmitters in the VLM that are associated
with changes in mean arterial pressure and heart rate during static muscle
contraction in anesthetized animals. Possible mechanisms in the VLM that mo
dulate cardiovascular changes during static muscle contraction are summariz
ed and discussed. Localized administration of an excitatory amino-acid anta
gonist into the rostral portion of the VLM (RVLM) attenuates increases in b
lood pressure and heart rate during static muscle contraction, whereas its
administration into the caudal part of the VLM (CVLM) augments these respon
ses. Opioid or 5-HT1A receptor stimulation in the RVLM, but not in the CVLM
, attenuates cardiovascular responses to muscle contraction. Furthermore, i
ntravenous, intracerebroventricular or intracisternal injection of an alpha
(2)-adrenoceptor agonist or a cholinesterase inhibitor attenuates increases
in blood pressure and heart rate during static muscle contraction. Finally
, the possible involvement of endogenous neurotransmitters in the RVLM and
the CVLM associated with cardiovascular responses during static muscle cont
raction is discussed. An overview of the role of the VLM in the overall car
diovascular control network in the brain is presented and critically review
ed. (C) 1998 Elsevier Science Ltd. All rights reserved.