The rostral ventrolateral medulla (RVLM), also known as the pressor area of the medulla, is a brain region that is responsible for basal and reflex control of sympathetic activity associated with cardiovascular function.[1] Abnormally elevated sympathetic activity in the RVLM is associated with various cardiovascular diseases, such as heart failure and hypertension.[1] The RVLM is notably involved in the baroreflex.

It receives inhibitory GABAergic input from the caudal ventrolateral medulla (CVLM). The RVLM is a primary regulator of the sympathetic nervous system; it sends catecholaminergic projections to the sympathetic preganglionic neurons in the intermediolateral nucleus of the spinal cord via reticulospinal tract.

Physostigmine, a choline-esterase inhibitor, elevates endogenous levels of acetylcholine and causes a rise in blood pressure by stimulation of the RVLM.[2] Orexinergic neurons from the lateral hypothalamus output in the RVLM.

See also

References

  1. 1 2 Mischel NA, Subramanian M, Dombrowski MD, Llewellyn-Smith IJ, Mueller PJ (May 2015). "(In)activity-related neuroplasticity in brainstem control of sympathetic outflow: unraveling underlying molecular, cellular, and anatomical mechanisms". Am. J. Physiol. Heart Circ. Physiol. 309 (2): H235–43. doi:10.1152/ajpheart.00929.2014. PMC 4504968. PMID 25957223. Specifically, we focus on changes in the rostral ventrolateral medulla (RVLM), a critical brain region for basal and reflex control of sympathetic activity. The RVLM is implicated in elevated sympathetic outflow associated with several cardiovascular diseases including hypertension and heart failure
  2. ↑ Medullary pressor area: site of action of intravenous physostigmine
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