Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation

Citation
Af. Sved et al., Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation, BRAIN RES B, 51(2), 2000, pp. 129-133
Citations number
38
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH BULLETIN
ISSN journal
03619230 → ACNP
Volume
51
Issue
2
Year of publication
2000
Pages
129 - 133
Database
ISI
SICI code
0361-9230(20000115)51:2<129:BDAIRO>2.0.ZU;2-0
Abstract
The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovasc ular regulation. Convincing data now support the hypothesis that inhibition of sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) by CVLM neurons constitutes the necessary inhibitory link in baroreceptor r eflex mediated control of sympathetic vasomotor outflow. Inhibition or dest ruction of the CVLM produces severe acute hypertension, consistent with blo ckade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympath oexcitatory neurons. However, other data indicate that the CVLM also tonica lly inhibits RVLM sympathoexcitatory neurons in a manner not driven by baro receptor input. In some studies, inhibition of the CVLM results in an incre ase in arterial pressure (AP) without inhibiting baroreceptor reflexes, pos sibly reflecting baroreceptor-independent and baroreceptor-dependent sub-re gions of the CVLM. Furthermore, in baroreceptor-denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontane ously hypertensive rats (SHR) central processing of baroreceptor reflexes a ppears normal but CVLM-mediated inhibition of the RVLM seems to be attenuat ed, suggesting that it is specifically a baroreceptor-independent mechanism of cardiovascular regulation in SHR that is altered. Taken together, these findings support an important, tonic, baroreceptor-independent inhibition of RVLM sympathoexcitatory neurons exerted by the CVLM. (C) 2000 Elsevier S cience Inc.