AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 2 519-R526, Copyright © 1994 by American Physiological Society
A5 noradrenergic neurons and the carotid sympathetic chemoreflex
N. Koshiya and P. G. Guyenet
Department of Pharmacology, University of Virginia Health Sciences Center, Charlottesville 22908.
Inhibition of neural activity in the caudal ventrolateral pons (A5 area) by
microinjection of muscimol (Mus) attenuates (-65%) the carotid sympathetic
chemoreflex (SChR) without altering the concomitant activation of the
phrenic nerve (PND). The present study, performed in urethan-anesthetized
rats, explores the possibility that activation of the noradrenergic (NE)
neurons of the A5 area is involved in the SChR. The NE neuron-selective
toxin 6-hydroxydopamine (6-OHDA) was microinjected bilaterally into the
spinal cord at T2 level (4 micrograms). This dose reduced the SChR by 55%
(n = 5) 90 min after injection, while 0.4 microgram of 6-OHDA produced no
effect (n = 5). In seven rats that had received 250 micrograms 6-OHDA
intracisternally 2 wk before, Mus injections into the A5 area failed to
attenuate the SChR. These rats also had a lower resting mean arterial
pressure than controls (97 vs. 112 mmHg). Spinal intrathecal injection of
alpha-adrenergic receptor antagonists (prazosin, 10 and 20 micrograms) or
phentolamine (20 and 40 micrograms) attenuated resting sympathetic nerve
discharge (SND) and SChR in a roughly proportional manner (25-40%); the
beta-adrenergic antagonist nadolol (10 and 20 microgram(s) intrathecally)
attenuated the SChR selectively but modestly (-10%). The results are
generally compatible with the hypothesis that A5 NE neurons and
particularly their spinal cord projection could play a facilitating role in
the SChR. However, clear evidence that A5 cells contribute selectively to
sympathoactivation during chemoreceptor stimulation by releasing NE in the
spinal cord could not be obtained.
