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Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.
Author(s) -
Potter E K
Publication year - 1981
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1981.sp013781
Subject(s) - baroreceptor , chemoreceptor , efferent , tonic (physiology) , medicine , vagus nerve , chloralose , anesthesia , reflex , heart rate , blood pressure , stimulation , afferent , receptor
1. Single and few‐fibre cardiac efferent filaments were dissected from the cervical vagus nerve of dogs anaesthetized with chloralose and paralysed with pancuronium. 2. Brief selective baroreceptor or chemoreceptor stimuli, given during the expiratory phase of the central respiratory cycle and while the lungs were motionless, evoked trains of action potentials in cardiac vagal efferent fibres. These vagal responses outlasted the duration of the stimuli by 1‐3 s. 3. Brief selective baroreceptor or chemoreceptor stimuli given during the inspiratory phase of the central respiratory cycle (monitored as phrenic discharge) but while the lungs were motionless, failed to evoke reflex increases in discharge. Background vagal discharge was also inhibited during central inspiratory activity. 4. Brief baroreceptor or chemoreceptor stimuli given during lung inflation but in the expiratory phase of the central respiratory cycle (phrenic silence), also failed to evoke any reflex increase in discharge, but left resting vagal tone relatively unaffected. Only when vagal tone was high was it markedly inhibited by lung inflation, in the absence of central inspiratory activity. 5. A point of contrast between the inhibitory effects of lung inflation and of central inspiratory activity is that both tonic and reflexly evoked vagal discharge are inhibited during central inspiratory activity, but lung inflation more markedly inhibits reflexly evoked vagal discharge than tonic vagal discharge. 6. A model is suggested to explain the different mechanisms of inhibition by lung inflation and by central inspiratory activity.

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