Supraspinal inhibition of a cutaneous vascular reflex in the cat

1964 ◽  
Vol 207 (2) ◽  
pp. 303-307 ◽  
Author(s):  
B. J. Prout ◽  
J. H. Coote ◽  
C. B. B. Downman

In cats anesthetized with chloralose-urethane mixture, stimulation of an afferent nerve evoked a vasoconstrictor reflex (VCR) and a galvanic skin response (GSR) in the pads of the feet. Stimulation of the ventromedial medullary reticular substance at the level of the obex abolished the VCR and the GSR. VCR could also be reduced by occlusion during prolonged stimulation of another spinal or visceral afferent pathway. Medulla stimulation was effective without itself causing a sympathetic discharge to the paw, showing that inhibition rather than occlusion was operative. Anterior cerebellar stimulation also inhibited the VCR. Carotid sinus nerve stimulation did not abolish the VCR. It is concluded that the effective mechanism includes a bulbospinal inhibitory path projecting on a spinal vasoconstrictor reflex arc. This arrangement is similar to the descending pathways inhibiting other spinal reflexes but the VCR-inhibitory path can be activated independently of them.

1983 ◽  
Vol 244 (3) ◽  
pp. H437-H443 ◽  
Author(s):  
R. B. Felder ◽  
C. M. Heesch ◽  
M. D. Thames

Carotid sinus baroreceptor (CBR) sensitivity may be increased by electrical stimulation of sympathetic nerves passing to the carotid sinus region. It remains unknown if reflexly induced changes in efferent sympathetic discharge affect CBR function. In 17 anesthetized dogs, we reflexly induced alterations in sympathetic discharge and recorded CBR activity originating from a vascularly isolated carotid sinus. The stimulus to the baroreceptors was pulsatile with constant mean and pulse pressure. Occlusion of the contralateral common carotid artery (n = 6) resulted in a reflex increase in arterial pressure (116 +/- 10 to 153 +/- 14 mmHg) and an increase (121 +/- 2% of control) in baroreceptor activity (P less than 0.05). Inferior vena caval occlusion (n = 6), which induced a reduction in arterial pressure (145 +/- 19 to 75 +/- 21 mmHg), also provoked an increase (141 +/- 10% of control) in baroreceptor discharge (P less than 0.05). Raising pressure (to 200 mmHg) in the contralateral carotid sinus (n = 7) resulted in a reflex decrease in arterial pressure (169 +/- 16 to 129 +/- 13 mmHg) and a reduction (82 +/- 3% of control) in baroreceptor activity (P less than 0.05). The changes in baroreceptor discharge were abolished by ipsilateral cervical sympathectomy or ganglionic blockade (n = 4). Our findings demonstrate that reflexly induced alterations in the activity of sympathetic fibers innervating the carotid sinuses can modulate baroreceptor discharge.


1987 ◽  
Vol 253 (5) ◽  
pp. H1127-H1135 ◽  
Author(s):  
R. B. Felder ◽  
C. M. Heesch

Bilateral carotid sinus nerve stimulation was used as a model for studying cardiovascular afferent interactions in the nucleus tractus solitarius (NTS) region of dorso-medial medulla. Extracellular action potential recordings were made from 69 single units, 33 of which were excited independently by both right and left carotid sinus nerves (CSNs). Fifteen of these were located in NTS. Peak latencies to electrical stimulation of NTS neurons were 17.7 +/- 2.1 ms to ipsilateral CSN and 20.9 +/- 1.5 ms to contralateral CSN. Summation of afferent input was routinely demonstrated. In 10 units in NTS, a conditioning stimulus applied to one CSN caused prolonged inhibition of the response to a test stimulus to the same or the other CSN. The duration of inhibition was dependent on the intensity of the conditioning stimulus, not on prior excitation of the unit by the conditioning stimulus. In five additional excitability testing experiments, we found limited evidence to suggest that primary afferent depolarization of the central fibers of one CSN by stimulation of the contralateral CSN might be contributing to this inhibitory interaction. The data suggest that the outcome of integrative interactions between right and left CSN inputs to NTS neurons may depend largely on the temporal sequence of convergent afferent impulses.


1994 ◽  
Vol 76 (2) ◽  
pp. 602-609 ◽  
Author(s):  
R. F. Fregosi

Experiments were designed to test two hypotheses regarding the influence of isocapnic hypoxia on the expiratory activity of the abdominal muscles: 1) brain hypoxia attenuates the increased drive to the abdominal muscles that is elicited by hypoxic stimulation of peripheral chemoreceptor afferents, and 2) activation of the abdominal muscles in hypoxia requires vagal afferent feedback. The measurements included inspired ventilation (VI) and the electromyogram (EMG) of the external and internal oblique and transversus abdominis muscles in 12 supine cats that were anesthetized with chloralose (50 mg/kg) and breathed spontaneously. Changes in respiratory drive were evoked with isocapnic hypoxia or electrical stimulation of a carotid sinus nerve. Although both stimuli increased abdominal motor output, carotid sinus nerve stimulation evoked a significantly greater increase in the external and internal oblique EMG than hypoxia when comparisons were made at an equivalent level of VI. Neither stimulus changed the abdominal EMG significantly after bilateral cervical vagotomy. Separate experiments revealed that, at a given level of VI, hypercapnia evoked a significantly greater increase in abdominal activity than isocapnic hypoxia. The results suggest that the increased drive to the abdominal muscles elicited by stimulation of the peripheral and central chemoreceptors can be antagonized by an inhibitory input that is triggered by brain hypoxia. Moreover the decrease in expiratory motor activity often observed during hypoxia in vagotomized animals is due to the removal of an excitatory mechanism that is mediated by vagal afferent feedback.


2011 ◽  
Vol 7 (2) ◽  
pp. 89 ◽  
Author(s):  
Maria Teresa La Rovere ◽  
Roberto Maestri ◽  
Gian Domenico Pinna ◽  
◽  
◽  
...  

The baroreflex mechanism has been recognised as a key part of cardiovascular regulation. Alterations in the baroreceptor-heart rate reflex (baroreflex sensitivity [BRS]) contribute to sympathetic–parasympathetic imbalance, playing a major role in the development and progression of many cardiovascular disorders. Therefore, the measurement of the baroreflex is a source of valuable information in the clinical management of cardiac disease patients. This article reviews the most relevant advances for the measurement of BRS and their clinical and prognostic implications. Novel therapeutic strategies, exploring the use of electrical stimulation of the carotid sinus, have been evaluated recently in experimental and preliminary clinical studies to lower blood pressure and to reduce the level of baroreflex-mediated sympathoexcitation in heart failure. A recent study has also shown that the implementation of an artificial baroreflex system to regulate sympathetic vasomotor tone automatically is feasible.


2020 ◽  
Vol 43 (10) ◽  
pp. 1057-1067 ◽  
Author(s):  
Gean Domingos-Souza ◽  
Fernanda Machado Santos-Almeida ◽  
César Arruda Meschiari ◽  
Nathanne S. Ferreira ◽  
Camila A. Pereira ◽  
...  

1996 ◽  
Vol 76 (3) ◽  
pp. 1896-1903 ◽  
Author(s):  
Y. Uchino ◽  
M. Sasaki ◽  
H. Sato ◽  
M. Imagawa ◽  
H. Suwa ◽  
...  

1. Intracellular recordings of synaptic potentials in extraocular motoneurons were studied to determine the connectivities between the utricular nerve and the extraocular motoneurons in cats. 2. Stimulating electrodes were placed within the left utricular nerve, while other branches of the vestibular nerve were removed. Subsequently, the N1 field potentials evoked by utricular nerve stimulation were recorded in the vestibular nuclei. The potential typically grew until reaching a plateau (submaximal stimulation). Stimulus spread to the other nerve branches appeared as an additional increase in N1 amplitude after the plateau discontinued (supramaximal stimulation). 3. Intracellular recordings were made from 200 identified motoneurons in the bilateral III, IV, and VI cranial nuclei. 4. Stimulation of the utricular nerve at submaximal intensity evoked a longer latency depolarizing and hyperpolarizing potentials in contra- and ipsilateral medial rectus motoneurons, respectively. Complex potentials with longer latencies also were recorded in ipsilateral inferior oblique and contralateral trochlear motoneurons after stimulation of the utricular nerve at a submaximal intensity. Monosynaptic and disynaptic connections between the utricular nerve and ipsilateral abducens motoneurons and interneurons were recorded as described previously. 5. The results of the present study confirm our initial findings that a disynaptic pathway from the utricular nerve to contralateral trochlear motoneurons is absent or very poorly developed, whereas polysynaptic circuits from the utricular nerve to inferior oblique and trochlear motoneurons may play a role in eye rotation during head tilt.


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