Spectral analysis was used to investigate variations of heart period in 13 decerebrate cats under different conditions of neural input to the heart. Spectral density plots in intact animals showed three well-defined peaks: P1 (1.5-2.5 cycles/min), P2 (6-10 cycles/min), and P2 (respiratory frequency). In the presence of sympathetic input only the amplitudes of all peaks were decreased; when only vagal input was present the amplitudes of P1 and P2 were increased and there was no change in P3; when neither sympathetic nor vagal input was present the amplitudes of all peaks were decreased. In addition, the amplitudes of P1 and P2 were increased and there was no change in P3; when neither sympathetic nor vagal input was present the amplitudes of all peaks were decreased. In addition, the amplitudes of P1 and P2 were found to be significantly correlated with the mean heart period under the condition of vagal control only. It is concluded that P3 is related to sinus arrhythmia and that P1 and P2 may be related to spontaneous rhythms that are an intrinsic feature of the dynamic regulation of heart period by the vagus system. Sympathetic activity plays no role in the genesis of these rhythms.

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Electrical stimulation of the amygdala has been shown to produce changes in cardiovascular variables. To locate neuronal cell bodies responsible for these changes, responses of arterial pressure (AP) and heart rate (HR) to DL-homocysteate (DLH, 0.15 M, 50-100 nl) microinjected into sites in three amygdaloid nuclei were compared with responses to electrical (90-150 microA) stimulation of the same sites in 35 artificially ventilated, paralyzed, urethan-anesthetized rats. Electrical stimulation resulted in depressor responses in most sites (89%). Changes in AP were accompanied by variable changes in HR. Chemical stimulation produced significantly fewer (25%) depressor responses. Similar results were obtained with injections of 1.0 M DLH. To eliminate the influence of the anesthetic on these responses, AP was recorded in nine conscious rats while stimulating the amygdala. Changes in behavior and AP in these animals could be obtained only by electrical stimulation. These results may be interpreted to indicate either that cell bodies responsible for changes in cardiovascular variables during electrical stimulation are not located in the amygdala or that chemical and electrical stimulation affect different neuronal elements in circuits located in the same anatomic site.