Hypertension, Vol 3, 240-244, Copyright © 1981 by American Heart Association
GR Hageman, F Urthaler, TN James and RH Swatzell Jr
Clonidine is an antihypertensive agent with a primary action mediated by
alpha adrenergic stimulation in the central nervous system, thus inhibiting
sympathetic efferent activity. Serotonin activates a cardiogenic
hypertensive chemoreflex which induces discharges of sympathetic efferent
neurons. The purpose of this study was to determine the effects of
intravenous clonidine upon the thoracic sympathetic efferent discharges in
chloralose-anesthetized dogs, their peripheral autonomic receptors being
blocked with atropine, propranolol, and phentolamine. Efferent nerve
traffic was quantified using a Schmitt trigger and Digital PDP8/e computer.
Control spontaneous activity (tone) following autonomic blockade was
normalized at 100%. Serotonin (100 microgram/ml, 2 ml, left atrium) caused
an increase in the reflex efferent sympathetic activity to 192% +/- 16% of
control (p less than 0.001). Following clonidine, the tone was decreased to
63% +/- 6% of control, and the reflex sympathetic discharge elicited by
serotonin was significantly (p less than 0.001) reduced from 192% to 116%
+/- 9% of control tone (before clonidine). The attenuation of the reflexly
elicited discharge was significantly (p less than 0.05) greater than the
attenuation of the tone. In four dogs that did not receive atropine, the
vago-vagal reflex sinus bradycardia induced by serotonin was not affected
by clonidine.
ARTICLES
Clonidine attenuation of a cardiogenic hypertensive chemoreflex
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