AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 6 1311-R1317, Copyright © 1993 by American Physiological Society
Coronary vasoconstrictor pathway from anterior hypothalamus includes neurons in RVLM
A. R. Goodson, T. S. LaMaster and D. D. Gutterman
Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City 52242.
We have previously identified discrete brain sites [anterior (AHA) and
lateral hypothalamus, periaqueductal gray, pontine parabrachial nucleus,
lateral reticular formation, and rostral ventrolateral medulla (RVLM)] in
the cat, in which electrical or chemical activation produces coronary
vasoconstriction. This study examines whether the most rostral (AHA) and
caudal (RVLM) of these sites are connected as part of a common pathway
mediating coronary vasoconstriction. In chloralose-anesthetized cats,
electrical stimulation in the AHA produced maximum increases in arterial
pressure (41 +/- 10%) and coronary vascular resistance (28 +/- 9%).
Microinjection of lidocaine into the RVLM attenuated the increases in
arterial pressure (10 +/- 3%) and coronary vascular resistance (5 +/- 1%)
in response to electrical stimulation in the AHA (P < 0.05 vs. before
lidocaine). Lidocaine nonspecifically inhibits neural elements in the
region. gamma-Aminobutyric acid in the RVLM, which selectively inhibits
cell bodies and not fibers passing through the RVLM, attenuated the
increase in coronary vascular resistance (38 +/- 8 to 14 +/- 3%; P <
0.05) but not the increase in arterial pressure (87 +/- 12 to 92 +/- 16%)
in response to electrical stimulation in the AHA. These data indicate that
coronary vasoconstriction in response to electrical stimulation in the AHA
requires cell bodies in the RVLM; however, the associated pressor response
is mediated by fibers passing through the RVLM. We conclude that a
polysynaptic descending pathway that mediates sympathetic coronary
vasoconstriction descends from the AHA through a synaptic connection in the
RVLM.
