A5 noradrenergic neurons and the carotid sympathetic chemoreflex

• Published in: The American journal of physiology Vol. 267; no. 2 Pt 2; pp. R519 - R526
• Main Authors: Koshiya, N, Guyenet, P G
• Format: Journal Article
• Language: English
• Published: United States 01-08-1994
• Subjects: Animals; Carotid Arteries - innervation; Chemoreceptor Cells - physiology; Injections, Spinal; Male; Neurons - physiology; Norepinephrine - physiology; Oxidopamine - pharmacology; Pons - cytology; Pons - physiology; Rats; Rats, Sprague-Dawley; Reflex - physiology; Spinal Cord - drug effects; Sympathetic Nervous System - physiology; Sympatholytics - pharmacology; Time Factors
• ISSN: 0002-9513
• DOI: 10.1152/ajpregu.1994.267.2.r519

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.