Cardiac receptors activated during the hypothalamic defence reaction.
The increases of arterial blood pressure, cardiac inotropy and venous return seen during the hypothalamic defence reaction are likely to lead to concomitant excitation of left ventricular receptors with nonmedullated afferents. The integrated efferent pattern of response resulting from the central interaction between the defence reaction and influences from the mentioned cardiac receptors was recently analyzed. These two, essentially opposing influences on the circulation were then seen to interact in such a way as to produce an optimal cardiovascular response with respect to increases in cardiac output and blood supply to the skeletal muscles. However, direct electrophysiological recordings from nonmedullated cardiac efferents during defence area stimulation have hitherto been lacking. The present experiments, performed on chloralose-anesthetized cats and utilizing electrophysiological recordings, clearly demonstrate that the left ventricular receptors are activated by the cardiovascular readjustments induced by the defence reaction. Defence area stimulation increased the activity of these receptors, which work within a very narrow, low frequency range, from 1.1 +/- 0.3 imp/s to 2.7 +/- 0.7  imp/s associated with rises in systolic blood pressure (afterload) and heart rate. Normally such a receptor activation would induce considerable bradycardia and sympathetic inhibition, but particularly the reflex bradycardia is centrally supressed by a concomitant defence area activation. The marked bradycardia  often seen immediately upon interruption of the defence area stimulation is, however, probably to a great extent initiated from the excited ventricular receptors.
D000818:Animals; D001794:Blood Pressure; D002415:Cats; D005260:Female; D006321:Heart / Q000294:innervation*; D006352:Heart Ventricles / Q000294:innervation; D007031:Hypothalamus / Q000502:physiology*; D008297:Male; D008465:Mechanoreceptors / Q000502:physiology*; D011311:Pressoreceptors / Q000502:physiology