TY - JOUR
T1 - Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation
AU - Sved, Alan F.
AU - Ito, Satoru
AU - Madden, Christopher J.
N1 - Funding Information:
Some of this work was supported by a grant from the National Institutes of Health (NIH) (no. HL55687). C. J. Madden was supported by funds from an NIH Training Grant (no. 5T32NS07391).
PY - 2000/1/15
Y1 - 2000/1/15
N2 - The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovascular 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 reflex mediated control of sympathetic vasomotor outflow. Inhibition or destruction of the CVLM produces severe acute hypertension, consistent with blockade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympathoexcitatory neurons. However, other data indicate that the CVLM also tonically inhibits RVLM sympathoexcitatory neurons in a manner not driven by baroreceptor input. In some studies, inhibition of the CVLM results in an increase in arterial pressure (AP) without inhibiting baroreceptor reflexes, possibly reflecting baroreceptor-independent and baroreceptor-dependent sub-regions of the CVLM. Furthermore, in baroreceptor- denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontaneously hypertensive rats (SHR) central processing of baroreceptor reflexes appears normal but CVLM-mediated inhibition of the RVLM seems to be attenuated, 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 Science Inc.
AB - The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovascular 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 reflex mediated control of sympathetic vasomotor outflow. Inhibition or destruction of the CVLM produces severe acute hypertension, consistent with blockade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympathoexcitatory neurons. However, other data indicate that the CVLM also tonically inhibits RVLM sympathoexcitatory neurons in a manner not driven by baroreceptor input. In some studies, inhibition of the CVLM results in an increase in arterial pressure (AP) without inhibiting baroreceptor reflexes, possibly reflecting baroreceptor-independent and baroreceptor-dependent sub-regions of the CVLM. Furthermore, in baroreceptor- denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontaneously hypertensive rats (SHR) central processing of baroreceptor reflexes appears normal but CVLM-mediated inhibition of the RVLM seems to be attenuated, 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 Science Inc.
KW - A1 area
KW - Baroreceptor
KW - Hypertension
KW - Spontaneously hypertensive rats
KW - Sympathoinhibition
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U2 - 10.1016/S0361-9230(99)00234-8
DO - 10.1016/S0361-9230(99)00234-8
M3 - Article
C2 - 10709958
AN - SCOPUS:0033972921
SN - 0361-9230
VL - 51
SP - 129
EP - 133
JO - Journal of Electrophysiological Techniques
JF - Journal of Electrophysiological Techniques
IS - 2
ER -