AJP - Heart and Circulatory Physiology, Vol 256, Issue 6 1601-H1608, Copyright © 1989 by American Physiological Society
Nodulus-uvula depressor response: central GABA-mediated inhibition of alpha-adrenergic outflow
R. T. Henry, J. D. Connor and C. D. Balaban
Department of Pharmacology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.
Electrical stimulation of a lateral region of the cerebellar nodulus-uvula
transition zone in anesthetized albino rabbits decreases mean arterial
blood pressure in direct proportion to stimulus intensity. The hypotension
has an abrupt onset and is phasic; heart rate is unaffected. Neural
pathways that might mediate the depressor response were studied using
autonomic-blocking agents. Pretreatment with 2 mg/kg iv of either
propranolol HCl or atropine methyl nitrate did not alter the onset or
duration of the hypotensive response. However, pretreatment with 2 mg/kg iv
phentolamine HCl abolished the depressor response, and 7 mg.kg-1.min-1 iv
tetraethylammonium infusion decreased the response by more than 50%.
Ipsilateral injections of 200 ng bicuculline methiodide into an area
immediately dorsal to the superior cerebellar peduncle or the dorsal aspect
of the superior vestibular nucleus reversibly attenuated the nodulus-uvula
evoked depression. Anterograde horseradish peroxidase-wheat germ agglutinin
(HRP-WGA) transport experiments revealed that both these regions receive
direct inputs from the nodulus-uvula. These data suggest that hypotensive
events elicited by lateral nodulus-uvula stimuli represent a central,
alpha-aminobutyric acid-mediated, phasic inhibition of vasomotor drive
mediated through autonomic ganglia to alpha-adrenoreceptors in the
vasculature.
