Respiratory modulation of baroreceptor and chemoreceptor reflexes affecting heart rate through the sympathetic nervous system

Abstract

Brief stimuli were delivered to the carotid body chemoreceptors or the carotid sinus baroreceptors at different phases of the respiratory cycle in anesthetized dogs. Chemoreceptor stimulation was achieved by injecting small volumes (0.2-0.5 ml) of warmed saline equilibrated with CO2 near the carotid bodies on both sides. Baroreceptor stimulation was achieved by injecting larger volumes (2-5 ml) of saline equilibrated with air into the region of the carotid bifurcation on both sides, after first clamping the common carotid arteries. When the vagus nerves were intact, but sympathetic nervous effects on heart rate were blocked by administration of propranolol, there was a prompt and pronounced bradycardia evoked when either baroreceptor or chemoreceptor stimuli were given in expiration, but little or no change in heart rate when they were given in inspiration. When the vagus nerves were cut, but sympathetic nervous function was intact, respiratory modulation of baroreceptor and chemoreceptor reflex effects on heart rate could still be demonstrated. The bradycardia evoked by either stimulus was more marked for stimuli given in expiration than for stimuli given in inspiration. A complementary response pattern for brief decreases in baroreceptor stimulation (carotid occlusions) was demonstrated: the tachycardia evoked by occlusions timed during inspiration was greater than that evoked by occlusions timed during expiration. All reflex effects were mediated by the sympathetic system because they were abolished by administration of propranolol. The sympathetic reflex effects were slight in comparison with the vagal reflexes evoked by either chemoreceptor or baroreceptor stimuli.