Journal of Neuroscience, Vol 9, 923-942, Copyright © 1989 by Society for Neuroscience
Cholinergic regulation of arterial pressure by the C1 area of the rostral ventrolateral medulla
R Giuliano, DA Ruggiero, S Morrison, P Ernsberger and DJ Reis
Division of Neurobiology, Cornell University Medical College, New York, New York 10021.
In anesthetized, paralyzed rats intravenous administration of the
acetylcholinesterase inhibitor physostigmine (PHY) (100 micrograms/kg)
evoked a dose-related rise in arterial pressure (AP) and heart rate (HR)
and an associated increase in sympathetic nerve activity (SNA). The
responses to PHY were blocked by electrolytic lesions of, or microinjection
of kainic acid into, a specific site in the rostral ventrolateral medulla
containing a cluster of neurons immunoreactive for the
adrenaline-synthesizing enzyme phenylethanolamine N- methyltransferase and
corresponding to the C1 area of the nucleus reticularis
rostroventrolateralis (RVL). The C1 area and its surround contain a
heretofore unrecognized network of varicose neuronal processes and
perikarya labeled immunocytochemically with a monoclonal antibody to the
ACh-synthesizing enzyme, choline acetyltransferase (CAT). PHY increased, by
over 3-fold, the spontaneous activity of reticulospinal cardiovascular
neurons in the C1 area which excite preganglionic sympathetic neurons in
the intermediolateral spinal column. The effects of PHY on AP, SNA, and the
discharge of reticulospinal neurons were blocked by systemic administration
of the muscarinic antagonist scopolamine. Microinjections within the C1
area of the RVL of scopolamine, the M2-selective muscarinic receptor
antagonist AF-DX 116, or the high-affinity choline uptake inhibitor
hemicholinium-3 blocked the pressor effects of PHY. The nicotinic
antagonist hexamethonium and the M1-selective muscarinic receptor
antagonist pirenzepine were without effect. We conclude that (1) the
increases in AP, HR, and SNA elicited by the systemic administration of PHY
result from the augmented action of ACh released from cholinergic terminals
within the C1 area of the RVL; (2) the locally released ACh acts through
muscarinic receptors of the M2 subtype within the C1 area to produce
excitation of intrinsic reticulospinal sympathoexcitatory neurons, thereby
increasing the activity of sympathetic preganglionic neurons and
consequently elevating AP and HR; and (3) while the specific function of
the cholinergic innervation of the C1 area in cardiovascular regulation is
unknown, it may contribute to the tonic regulation of AP.
Previous Article | Next Article
