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1 Department of Anesthesiology and 2 Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157
Ischemic stimulation of cardiac
receptors reflexly excites the cardiovascular system. However, the
supraspinal mechanisms involved in this reflex are not well defined.
This study examined the responses of barosensitive neurons in the
rostral ventrolateral medulla (RVLM) to stimulation of cardiac
receptors and the afferent pathways involved in these responses.
Single-unit activity of RVLM neurons was recorded in
-chloralose-anesthetized rats. Cardiac receptors were stimulated by
epicardial application of 10 µg/ml of bradykinin (BK). Barosensitive
neurons were silenced by stimulation of baroreceptors. Application of
BK increased the mean arterial pressure from 65.2 ± 1.9 to
89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from
6.2 ± 0.7 to 10.7 ± 0.9 impulses/s (P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive
neurons. Blockade of stellate ganglia abolished the response of
barosensitive neurons to BK. Cervical vagotomy significantly increased
the baseline discharges of RVLM barosensitive neurons but had no effect
on their responses to BK. Thus this study indicates that stimulation of
cardiac receptors selectively activates RVLM barosensitive neurons
through sympathetic afferent pathways. This information suggests that
the RVLM barosensitive neurons are likely involved in the sympathetic
control of circulation during myocardial ischemia.
cardiac nociceptors; angina pectoris; afferent neurons; sympathetic nervous system; cardiovascular reflexes; myocardial ischemia
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