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The goal of this study was to determine if physiological levels of cardiopulmonary vagal afferent activity modulate carotid chemoreceptor and baroreceptor reflexes. In anesthetized, ventilated dogs, the aortic nerves and the cervical sympathetic trunks were cut, and atropine was administered so that vagotomy would interrupt only cardiopulmonary afferent impulses. Reflex vascular responses were observed in perfused gracilis muscle and hindpaw. Carotid chemoreceptors were activated with nicotine or hypoxic, hypercapnic blood; carotid baroreceptors were stimulated by changes in carotid pressure. Interruption of vaga afferents augmented reflex vascular responses during changes incarotid pressure from 75 to 125 mm Hg. Interruption of cardiopulmonary vagal afferents potentiated reflex vasoconstrictor (muscle), vasodilator (paw), and vasopressor responses to activation of the carotid chemoreceptors. The potentiation of the chemoreceptor reflex frequently occurred in the absence of increases in base-line vascular resistance. Vagotomy also potentiated ventilatory responses to stimulation of the carotid chemoreceptors in spontaneously breathing dogs. The results indicate that interruption of cardiopulmonary afferents potentiates the vascular and ventilatory responses to activation of the carotid chemoreceptors and augments the gain of the carotid baroreceptor reflex at low carotid pressures. These findings suggest that physiological levels of cardiopulmonary vagal afferent impulses suppress carotid baroreceptor and chemoreceptor reflexes through an interaction in the central nervous system. The suppressive effect on the chemoreceptor reflex may be distinct from tonic restraint of the vasomotor center by vagal afferents, since it involves sympathetic vasodilator as well as vasoconstrictor responses and may occur without suppression of base-line adrenergic constrictor tone.

Influence of cardiopulmonary vagal afferent activity on carotid chemoreceptor and baroreceptor reflexes in the dog.