AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 2 508-R518, Copyright © 1994 by American Physiological Society
Role of the pons in the carotid sympathetic chemoreflex
N. Koshiya and P. G. Guyenet
Department of Pharmacology, University of Virginia Health Sciences Center, Charlottesville 22908.
The mass discharges of the splanchnic sympathetic (SND) and phrenic nerves
(PND) were recorded in urethananesthetized rats with resected vagal and
aortic nerves. Carotid chemoreceptor (CC) stimulation with N2 inhalation
(4-12 s) or cyanide (50-100 micrograms/kg iv) activated SND in bursts
synchronized with the postinspiratory phase (mean SND increase: 105 +/-
8%), raised AP, and increased PND rate and amplitude (n = 40). Brain
transection at superior collicular level produced no effect. The
sympathetic (SChR) and respiratory chemoreflexes (RChR) were reduced after
transections through the pons. Lesions of the dorsolateral pons (dl-pons)
produced CO2-dependent apneusis and/or tachypnea at rest. After such
lesions, CC stimulation produced expiratory apnea and a 30% increase in
SChR due to tonic activation of SND. In contrast, bilateral lesions of the
ventrolateral pons (vl-pons) reduced the SChR by 54-76%. Muscimol (Mus)
injections (bilateral, 175 pmol/side) into vl-pons did not change resting
SND, MAP, baroreflex, and RChR but reduced the SChR (54-82%). In
conclusion, under anesthesia: 1) the pathway of the carotid chemoreflex is
confined to the pons and medulla, 2) the dl-pons exerts indirect control
over the SChR via its role in respiratory rhythmogenesis, and 3) neurons in
the vl-pons contribute selectively to the SChR but not to PND activation
during CC activation.
