Mj. Drinkhill et al., DELAYED SYMPATHETIC EFFERENT RESPONSES TO CORONARY BARORECEPTOR UNLOADING IN ANESTHETIZED DOGS, Journal of physiology, 497(1), 1996, pp. 261-269
1. We previously reported that, although stimulation of coronary arter
ial baroreceptors results in reflex vasodilatation of a magnitude and
a time course similar to that seen in response to carotid baroreceptor
stimulation, the vasoconstriction that occurs when the stimulus to co
ronary baroreceptors is removed develops more slowly. We now report th
e results of experiments designed to investigate the site on the refle
x are that is responsible for the delayed vasoconstriction. 2. In alph
a-chloralose anaesthetized, artificially ventilated dogs, a perfusion
circuit allowed independent control of pressures to the aortic root, i
ncluding the coronary arteries, the aortic arch and the carotid sinuse
s. Electrophysiological recordings were made of afferent discharge in
nerve fibres dissected from the vagus nerve, which responded to change
s in coronary pressure, and from renal and lumbar efferent sympathetic
nerves. Reflex vascular responses were assessed from changes in perfu
sion pressure to the systemic circulation, which was perfused at const
ant flow. 3. The afferent discharge from the coronary baroreceptors re
sponded rapidly to both increases and decreases in coronary perfusion
pressure. This indicates that prolonged activation of the coronary rec
eptors cannot be the cause of the delayed vasoconstriction. 4. An incr
ease in pressure to the coronary baroreceptors resulted in an immediat
e decrease in activity in either renal or lumbar sympathetic nerves. A
decrease in coronary pressure, however, was followed by a slow gradua
l increase in sympathetic discharge. This contrasts with the responses
to decreases in carotid or aortic arch pressures, which were followed
by rapid increases in efferent discharge, often with an overshoot. 5.
We conclude that the slow recovery of efferent sympathetic activity f
ollowing a reduction in coronary pressure is likely to explain the pre
viously reported slow recovery of vascular resistance.