Respiratory modulation of sympathetic activity.
Sympathetic activity recorded from cardiac and renal nerves was correlated with phrenic and internal intercostal nerve activity under normocapnea and hypercapnea. Cats were anesthetized with halothane for surgery switching to chloralose for recording. Both vagal and carotid sinus nerves were cut, animals were paralyzed and artificially ventilated. We found that sympathetic activity followed the rhythmic pattern of phrenic nerve discharge fairly closely except in two important respects: first, sympathetic activity was significantly depressed during early inspiration and second, it reached a minimum during post inspiration while phrenic activity was decaying but still active. These effects were accentuated when PACO2 was raised. In one cat early inspiratory depression was the only manifestation of respiratory modulation of sympathetic activity superimposed on an otherwise tonic pattern. In 4 cats sympathetic activity increased in an augmenting fashion in parallel with the augmenting discharge of expiratory alpha motoneurones. We suggest that respiratory-related, excitatory and inhibitory inputs modulate sympathetic activity at the brainstem level. Inspiratory and possibly expiratory interneurones may be the source of activation, and inhibitory inputs may derive from early inspiratory and postinspiratory interneurones. The inhibitory effects may be the only manifestation of respiratory modulation during strong tonic drive of the sympathetic activity.
D000818:Animals; D001933:Brain Stem / Q000502:physiology; D002415:Cats; D005260:Female; D006321:Heart / Q000294:innervation*; D007367:Intercostal Nerves / Q000502:physiology; D007668:Kidney / Q000294:innervation*; D008297:Male; D009046:Motor Neurons / Q000502:physiology; D009433:Neural Inhibition; D010791:Phrenic Nerve / Q000502:physiology; D012119:Respiration; D013564:Sympathetic Nervous System / Q000502:physiology*