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Link to original content: http://pubmed.ncbi.nlm.nih.gov/17184513/
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Review
. 2006 Dec;33(12):1265-8.
doi: 10.1111/j.1440-1681.2006.04522.x.

Differential control of cardiac and sympathetic vasomotor activity from the dorsomedial hypothalamus

J Horiuchi  1 , L M McDowall, R A L Dampney
Affiliations
Review

Differential control of cardiac and sympathetic vasomotor activity from the dorsomedial hypothalamus

J Horiuchi et al. Clin Exp Pharmacol Physiol. 2006 Dec.

Abstract

1. The dorsomedial hypothalamus (DMH) plays a crucial role in mediating the cardiovascular responses to different stressors, including acute psychological stress and cold stress. Activation of neurons in the DMH evokes increases in arterial pressure and in the activity of sympathetic nerves innervating the heart, blood vessels and brown adipose tissue. The descending pathways from the DMH to the spinal sympathetic outflow include synapses with neurons in medullary nuclei and possibly other brain stem regions. 2. Recent studies from our and other laboratories have indicated that neurons in the rostral ventrolateral medulla (RVLM) and in the region of the raphe pallidus (RP) in the medulla are important components of the descending pathways that mediate the cardiovascular response to activation of the DMH. Neurons in the RP primarily mediate the sympathetic cardiac components of the DMH-evoked response, whereas the RVLM neurons primarily mediate the sympathetic vasomotor component. 3. Activation of DMH neurons not only increases heart rate and sympathetic vasomotor activity, but also resets the baroreceptor reflex such that it remains effective, without any decrease in sensitivity, over a higher operating range of arterial pressure. 4. Activation of 5-hydroxytryptamine 5-HT(1A) receptors in the medulla oblongata leads to a selective suppression of cardiac and sympathetic vasomotor components of the DMH-evoked response, but does not affect sympathetic reflex responses evoked from baroreceptors or chemoreceptors. Thus, central 5-HT(1A) receptors modulate cardiovascular responses evoked from the DMH in a highly potent but selective fashion.

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