Action potentials from ventricular mechanoreceptors stimulated by occlusion of the coronary sinus in the dog.
1. In experiments to determine the type of intra-cardiac receptors which cause the coronary sinus occlusion reflex, recordings were made from sixty-nine single and small multi-fibre preparations of cardiac vagal afferents in open-chest anaesthetized dogs.2. Thirty-two fibres were stimulated by occlusion of the coronary sinus outflow through an indwelling Morawitz cannula. No receptors were stimulated during occlusions at peak systolic coronary venous pressures below the threshold for reflex cardiovascular depression. At higher pressures, fibre recruitment and further increases in stimulated discharge were demonstrated.3. The afferent endings of twenty-nine of these fibres were mechanically localized to the epicardium and myocardium of the left ventricle. Three were in the right ventricle. Seventeen single fibres discharged spontaneously at an average of 0.9 impulses/sec. There was cardiac modulation of both resting and stimulated discharge, with most action potentials in systole. Seven of eight fibres conducted at less than 1.0 m/sec.4. These ventricular receptors and a further twenty-two otherwise like them but not stimulated by occlusions were designated epi-myocardial receptors.5. 73% of receptors were stimulated by intrapericardial nicotine (50-100 mug). Presumptively superficial receptors were more sensitive to this stimulus.6. Epi-myocardial receptors were stimulated by intravenous or intracoronary catecholamines, by electrical stimulation of cardiac sympathetic nerves, and by eliciting the carotid sinus occlusion reflex. Aortic occlusion stimulated 66% of fibres tested, but was a less effective stimulus. After all these stimuli, there was a systolic modulation of discharge in more than 70% of fibres.7. It was concluded that the epi-myocardial receptors are similar to those previously shown to cause the epicardial chemoreflex, and to participate in the coronary chemoreflex. It is suggested that they are responsive to systolic mechanical changes which are accentuated by catecholamines. Their possible effectiveness in other cardiac reflexes and in initiating circulatory changes at the beginning of exercise and the vasovagal syndrome is discussed.
D000200:Action Potentials; D000818:Animals; D001794:Blood Pressure; D003331:Coronary Vessels / Q000502:physiology*; D004285:Dogs; D004558:Electric Stimulation; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D005263:Femoral Artery; D006321:Heart / Q000294:innervation*; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000294:innervation; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D008465:Mechanoreceptors / Q000187:drug effects / Q000502:physiology*; D009431:Neural Conduction; D009475:Neurons, Afferent / Q000502:physiology; D009538:Nicotine / Q000494:pharmacology; D014690:Venous Pressure
D009538:Nicotine; D007545:Isoproterenol; D004837:Epinephrine