Interaction between carotid sinus baroreceptor and aortic nerve pressor reflexes in the dog

1979 ◽  
Vol 237 (6) ◽  
pp. H662-H667
Author(s):  
J. E. Kendrick ◽  
G. L. Matson

In dogs anesthetized with morphine-chloralose, strong, low-frequency (2 Hz) electrical stimulation of the aortic nerve (AN) causes pressure in the perfused hindlimbs to rise. This pressor response is followed by a large depressor phase upon cessation of stimulation. Simultaneous stimulation of the ipsilateral carotid sinus nerve (CSN) with intermittent trains of stimuli enhanced the AN pressor response by 113%. Similar stimulation of the contralateral CSN had little effect on the AN pressor response. Constant-frequency stimulation of the ipsilateral CSN also failed to enhance this response. Possible mechanisms of the interaction between these antagonistic reflexes were investigated. The results suggest that the augmentation of the AN pressor response results from a central neuronal interaction between these antagonistic reflexes.

1991 ◽  
Vol 70 (6) ◽  
pp. 2539-2550 ◽  
Author(s):  
F. A. Hopp ◽  
J. L. Seagard ◽  
J. Bajic ◽  
E. J. Zuperku

Respiratory responses arising from both chemical stimulation of vascularly isolated aortic body (AB) and carotid body (CB) chemoreceptors and electrical stimulation of aortic nerve (AN) and carotid sinus nerve (CSN) afferents were compared in the anesthetized dog. Respiratory reflexes were measured as changes in inspiratory duration (TI), expiratory duration (TE), and peak averaged phrenic nerve activity (PPNG). Tonic AN and AB stimulations shortened TI and TE with no change in PPNG, while tonic CSN and CB stimulations shortened TE, increased PPNG, and transiently lengthened TI. Phasic AB and AN stimulations throughout inspiration shortened TI with no changes in PPNG or the following TE; however, similar phasic stimulations of the CB and CSN increased both TI and PPNG and decreased the following TE. Phasic AN stimulation during expiration decreased TE and the following TI with no change in PPNG. Similar stimulations of the CB and CSN decreased TE; however, the following TI and PPNG were increased. These findings differ from those found in the cat and suggest that aortic chemoreceptors affect mainly phase timing, while carotid chemoreceptors affect both timing and respiratory drive.


1969 ◽  
Vol 49 (3) ◽  
pp. 589-596 ◽  
Author(s):  
Victor Parsonnet ◽  
Edwin L. Rothfeld ◽  
K. Venkata Raman ◽  
George H. Myers

1980 ◽  
Vol 59 (s6) ◽  
pp. 255s-257s ◽  
Author(s):  
Karen L. Barnes ◽  
C. M. Ferrario

1. The mechanism by which the area postrema augments central sympathetic drive during electrical stimulation is presently unknown. This pathway may involve either direct facilitation of brain-stem vasomotor neurons or inhibition of the sympatho-inhibitory baroreceptor relay in the nucleus tractus solitarii. 2. The present study employed selective lesions within the solitary tract nucleus to assess the participation of the primary baroreceptor relay in the pressor response during electrical stimulation of the area postrema. 3. The magnitude of the pressor response was unchanged after destruction of the solitary tract and lateral solitary nucleus which centrally interrupted the baroreceptor reflex. However, microknife cuts through the medial solitary nucleus, which spared the carotid sinus reflex, significantly reduced the magnitude of the area postrema pressor response. 4. Previous anatomical studies support these results and confirm that, although the area postrema pressor pathway traverses the most medial portion of the solitary complex, it does not produce augmented sympathetic outflow by inhibition of the primary baroreflex relay.


1960 ◽  
Vol 37 (4) ◽  
pp. 812-831
Author(s):  
D. W. EWER

1. The responses to electrical stimulation of isolated rings of the column and pedal disk of Calliactis are described. Such rings make slow spontaneous contractions which are frequently rhythmical, the interval between contractions normally being 7-20 min. 2. Continuous low-frequency stimulation inhibits spontaneous activity of rings from the pedal disk and also of fresh rings from more adoral regions of the column. Older rings from the mid-column respond to such stimulation by a tetanic contraction. 3. The latency of response to electrical stimulation of pedal rings is of the order of 120 sec. This latency is not affected by stimulation frequency but is prolonged by increase in the number of shocks applied. 4. Stimulation of a pedal ring at the onset of a contraction prevents the further development of this contraction, while stimulation as a contraction reaches its maximum is followed by more rapid relaxation than in unstimulated controls. 5. Mid-column rings when freshly prepared show a latency of the order of 120 sec. As the preparation ages, a double response to stimulation appears; the first response has a latency of about 30-40 sec. and presently becomes the only type of response shown. 6. If two sets of stimuli are applied to a mid-column ring, the magnitude of response to the second set increases as the time between stimulations increases. With long intervals an almost total contraction is obtained in response to a single shock. 7. The effect of intercalated stimuli upon the rhythm of spontaneous activity is studied. The effect is very variable and it is suggested that this is the result of electrical stimulation having both an excitatory and an inhibitory effect. 8. The very long latent periods characteristic of pedal rings and the rhythmic activity of these preparations are interpreted as interactions of excitation and inhibition.


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