Delayed sympathetic efferent responses to coronary baroreceptor unloading in anaesthetized dogs.
1. We previously reported that, although stimulation of coronary arterial 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 coronary baroreceptors is removed develops more slowly. We now report the results of experiments designed to investigate the site on the reflex are that is responsible for the delayed vasoconstriction. 2. In alpha-chloralose anaesthetized, artificially ventilated dogs, a perfusion circuit allowed independent control of pressures to the aortic root, including the coronary arteries, the aortic arch and the carotid sinuses. Electrophysiological recordings were made of afferent discharge in nerve fibres dissected from the vagus nerve, which responded to changes in coronary pressure, and from renal and lumbar efferent sympathetic nerves. Reflex vascular responses were assessed from changes in perfusion pressure to the systemic circulation, which was perfused at constant flow. 3. The afferent discharge from the coronary baroreceptors responded rapidly to both increases and decreases in coronary perfusion pressure. This indicates that prolonged activation of the coronary receptors cannot be the cause of the delayed vasoconstriction. 4. An increase in pressure to the coronary baroreceptors resulted in an immediate decrease in activity in either renal or lumbar sympathetic nerves. A decrease in coronary pressure, however, was followed by a slow gradual 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 following a reduction in coronary pressure is likely to explain the previously reported slow recovery of vascular resistance.
Drinkhill
M J
MJ
Institute for Cardiovascular Research, Research School of Medicine, University of Leeds, UK. cvsmjd@leeds.ac.uk
McMahon
N C
NC
Hainsworth
R
R
D000200:Action Potentials; D018686:Anesthetics, Intravenous / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000378:metabolism; D002698:Chloralose / Q000494:pharmacology; D004285:Dogs; D004525:Efferent Pathways / Q000502:physiology*; D004594:Electrophysiology; D005260:Female; D006321:Heart / Q000502:physiology*; D008297:Male; D010477:Perfusion / Q000379:methods; D011311:Pressoreceptors / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology*
D018686:Anesthetics, Intravenous; D002698:Chloralose