AJP - Regulatory, Integrative and Comparative Physiology, Vol 250, Issue 5 932-R945, Copyright © 1986 by American Physiological Society
Neurons of C1 area mediate cardiovascular responses initiated from ventral medullary surface
E. E. Benarroch, A. R. Granata, D. A. Ruggiero, D. H. Park and D. J. Reis
We sought to establish whether neurons of the C1 area of the rostral
ventrolateral medulla (RVL) mediate changes in arterial pressure and heart
rate evoked by topical application of drugs to the ventral medullary
surface of the rat. Animals were anesthetized, paralyzed, and ventilated.
The ventral surface was mapped with L-glutamate, and a restricted zone was
identified from which L-glutamate, as well as kainic acid, bicuculline,
strychnine, carbachol, or physostigmine, increased arterial pressure and
heart rate. The hypertensive effects of carbachol and physostigmine were
blocked by previous local application of atropine but not hexamethonium.
Application of gamma-aminobutyric acid (GABA) or glycine to this area
produced hypotension and bradycardia. Located caudal to the trapezoid
bodies and lateral to the pyramids, this area corresponded to points with
lowest threshold for pressor responses evoked by electrical stimulation and
overlapped the distribution of epinephrine-synthesizing cells of the RVL.
Processes arising from these neurons were identified reaching and
contacting the ventral surface. Unilateral lesions involving the C1 area or
phenylethanolamine-N-methyltransferase-labeled descending axons derived
from this area imparied by greater than 70% the response to ipsilateral
application of L-glutamate, GABA, or glycine to the ventral surface. We
suggest that neurons within the C1 area of RVL adjacent to or including
epinephrine cells may mediate cardiovascular changes elicited from a
restricted chemosensitive zone of the ventral medullary surface of the rat.
