A role for the ventral surface of the medulla in regulation of nasal resistance
M. A. Haxhiu, K. P. Strohl, M. P. Norcia, E. van Lunteren, E. C. Deal Jr and N. S. Cherniack
Nasal resistance is known to be affected by changes in nasal blood volume and hence to depend on sympathetic discharge to nasal blood vessels.
Structures located superficially near the ventrolateral surface of the
medulla significantly affect respiratory and sympathetic activity and the
tone of the trachea. To assess the importance of these structures on nasal
patency, we measured transnasal pressure at a constant flow and examined
the change in pressure produced by topically applied N-methyl-D-aspartic
acid (NMDA). Experiments were performed in chloralose-anesthetized,
paralyzed, and artificially ventilated cats. NMDA administered on the
intermediate area of the ventral surface of the medulla decreased
transnasal pressure and increased phrenic nerve activity. The response to
NMDA could be diminished or abolished by application to the ventral
medullary surface of the NMDA antagonist 2-amino-5-phosphonovalerate
(2-APV) or the local anesthetic lidocaine. Carotid sinus denervation and
posthypothalamic decerebration did not alter the nasal and phrenic nerve
responses to NMDA; however,
cervical sympathetic denervation decreased these responses, both in intact and in bilaterally adrenalectomized animals. Therefore, activation of NMDA receptors on structures near the ventral surface of the medulla increases tone in the nasal vasculature and leads to a response pattern that includes changes in not only phrenic nerve activity and blood pressure but also nasal patency.
http://ajpregu.physiology.org/cgi/content/abstract/253/3/R494 Am J Physiol Regul Integr Comp Physiol 253: R494-R500, 1987;
0363-6119/87 $5.00
AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 3 494-R500, Copyright © 1987 by American Physiological Society
-adrenergic receptors in primary afferent neurons to result from an altered gene expression triggered by cytokines/growth factors produced by disconnection of peripheral nerve fibers from their cell bodies. These additional adrenergic receptors are suggested to make nociceptors and other primary afferent neurons excitable by local or circulating norepinephrine and epinephrine. For central pathways, the adrenergic excitation would be equivalent to that produced by noxious events and would consequently evoke pain. In support, evidence is cited for a form of denervation supersensitivity in causalgia and for increased expression of human 
