scholarly journals THE RESPONSE IN EFFERENT CARDIAC SYMPATHETIC NERVES TO STIMULATION OF ATRIAL RECEPTORS, CAROTID SINUS BARORECEPTORS AND CAROTID CHEMORECEPTORS

1982 ◽  
Vol 67 (1) ◽  
pp. 151-163 ◽  
Author(s):  
R. J. Linden ◽  
D. A. S. G. Mary ◽  
D. Weatherill
1981 ◽  
Vol 240 (4) ◽  
pp. H650-H658 ◽  
Author(s):  
E. Tomomatsu ◽  
K. Nishi

Effects of electrical stimulation of sympathetic nerves to the carotid sinus on the discharge of single active baroreceptor fibers of the rabbit were examined in situ and in functionally isolated carotid sinus preparations with an intact sympathetic innervation under controlled conditions of pressure and temperature. Among 30 single units, 18 units responded to sympathetic stimulation of increasing discharge frequency. The excitatory effect of sympathetic stimulation on baroreceptor activity was not abolished by phentolamine (1 mg/kg iv or 10(-6) g/ml in perfusate). In isolated carotid sinus preparations perfused with Krebs-Henseleit solution, various pressure steps were applied to the sinus, and effects of norepinephrine (NE; 10(-9) and 10(-6) g/ml) on activity of nine single baroreceptor units were examined. In the presence of 10(-9) g/ml NE, discharge frequency of all units significantly increased at a given pressure step when compared with the control, whereas NE at a high concentration (10(-6) g/ml) did not produce significant changes in the discharge frequency. It is concluded that NE released by sympathetic nerve endings most likely acts directly on the baroreceptor nerve endings and sensitizes them.


1998 ◽  
Vol 79 (5) ◽  
pp. 2374-2382 ◽  
Author(s):  
L. Silva-Carvalho ◽  
J.F.R. Paton ◽  
I. Rocha ◽  
G. E. Goldsmith ◽  
K. M. Spyer

Silva-Carvalho, L., J.F.R. Paton, I. Rocha, G. E. Goldsmith and K. M. Spyer. Convergence properties of solitary tract neurons responsive to cardiac receptor stimulation in the anesthetized cat. J. Neurophysiol. 79: 2374–2382, 1998. The convergence pattern of cardiac receptors, pulmonary C-fibers, carotid chemoreceptor, and baroreceptor afferents onto neurons within the nucleus of the solitary tract (NTS) was studied in the anesthetized (pentobarbitone sodium, 40 mg/kg,) paralyzed and artificially ventilated cat. Extra- and intracellular recordings were made from NTS neurons while stimulating both cardiac receptors by aortic root injections of veratridine (1–3 μg/kg) and pulmonary C-fibers by a right atrial injection of phenylbiguanide (10–20 μg/kg). The ipsilateral carotid body was stimulated by using arterial injection of CO2-saturated bicarbonate solution, whereas inflation of the ipsilateral carotid sinus was used to activate baroreceptors. The ipsilateral cardiac vagal branch, cervical vagus, and carotid sinus nerves were stimulated electrically (1 Hz, 0.2–1 ms, 1–35 V). In 78 NTS neurons recorded either extracellularly ( n = 47) or intracellularly ( n = 31), electrical stimulation of the cardiac branch of the vagus nerve evoked synaptic potentials (spikes and/or excitatory postsynaptic potentials) with an onset latency between 4 and 220 ms. Some neurons displayed both short and long latency inputs(15.5 ± 1.8 and 160.0 ± 8.5 ms; n = 14). Of these 78 neurons, 24 responded to veratridine stimulation of cardiac receptors (i.e., cardioreceptive neurons) by exhibiting an augmenting–decrementing discharge of 37 ± 4 s in duration with a peak frequency of 30 ± 5 Hz. Convergence from other cardiorespiratory receptors was noted involving either carotid chemoreceptors ( n = 7) or pulmonary C-fibers ( n = 4) or from both carotid chemoreceptors and pulmonary C-fibers ( n = 6). In contrast, only one cardioreceptive NTS neuron was activated by distension of the carotid sinus. Recording sites recovered were confined to the medial NTS at the level of the area postrema and extended caudally into the commissural subnucleus. Our results indicate a convergence of carotid chemoreceptor and pulmonary C-fiber afferent inputs to cardioreceptive NTS neurons. With the paucity of baroreceptor inputs to these neurons it is suggested that sensory integration within the NTS may reflect regulatory versus defensive or protective reflex control.


Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Pedro L Katayama ◽  
Jaci A Castania ◽  
Rubens Fazan ◽  
Helio C Salgado

The mechanisms involved in Baroreflex Activation Therapy (BAT) in patients with resistant hypertension require better understanding. It was shown that electrical stimulation of the carotid sinus (ESCS), in conscious carotid body-denervated rats, caused bradycardia and greater hypotensive response when compared with intact control rats. In the current study the activation of the chemoreceptors due to ESCS, in conscious rats, was examined in the absence of the carotid baroreceptors. Wistar rats with unilateral denervation of the right carotid chemoreceptors were divided into three groups: 1) control (CONT, n=7); 2) bilateral carotid chemoreceptor denervation (CD, n=7); 3) unilateral denervation of the left carotid baroreceptors (BD, n=4). Under ketamine/xylazine anesthesia bipolar electrodes were implanted around the left carotid sinus combined with arterial and venous catheters into the femoral vessels. On the next day, after basal hemodynamic recordings, the animals received three ESCS (5V, 1 ms) with 15 Hz, 30 Hz and 60 Hz, applied randomly for 20s. Carotid chemoreceptors denervation was confirmed by the lack of hemodynamic responses after the administration of KCN (40 μg iv). The efficacy of left carotid baroreceptor denervation was confirmed by the absence of hemodynamic responses to changes in the left carotid sinus pressure ranging from 60 mmHg to 180 mmHg. The results showed that ESCS was efficient to cause greater hypotensive responses in the CD as compared with the CONT group at 60 Hz (-37 ± 6 vs -19 ± 3 mmHg) and to cause hypertensive responses in the BD group at 30 Hz and 60 Hz (15 ± 2 and 19 ± 2 mmHg). ESCS caused no alteration of the heart rate in the CONT but caused significant bradycardia in the CD group at 30 Hz and 60 Hz (-31 ± 11 and -35 ± 12 bpm) and in the BD group at 15 Hz, 30 Hz and 60 Hz (-38 ± 6, -37 ± 6 and -34 ± 4 bpm). These data demonstrated that carotid chemoreceptor activation in the absence of the carotid baroreceptors caused hypertension and bradycardia, indicating that when the baroreceptors are intact, the chemoreceptors blunt the hypotensive response caused by ESCS. These findings provide important information for the clinical studies using BAT in patients with resistant hypertension and/or heart failure.


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.


1982 ◽  
Vol 52 (5) ◽  
pp. 1261-1265 ◽  
Author(s):  
T. Nishino ◽  
A. Mokashi ◽  
S. Lahiri

Small doses of doxapram (less than 0.5 mg . kg-1 iv) were used to study its effect on carotid chemoreceptor activity and ventilation in cats anesthesized with alpha-chloralose. The effects were studied at several levels of partial pressures of O2 and CO2 in arterial blood (PaO2 and PaCO2). It was found that doxapram stimulated discharge rate of the carotid chemoreceptor afferents by the same magnitude at all levels of PaO2 and PaCO2 studied. However, the ventilatory effect of doxapram was more than additive to the concomitant stimulation by hypoxia or hypercapnia. This ventilatory effect was eliminated by sectioning the carotid sinus and aortic nerves. These results led to the conclusion that the ventilatory stimulus interaction due to doxapram is dependent on the excitatory input from the peripheral chemoreceptors.


1992 ◽  
Vol 73 (6) ◽  
pp. 2420-2424 ◽  
Author(s):  
R. A. Linton ◽  
D. M. Band ◽  
C. B. Wolff

It is known that during exercise there is an increase in plasma epinephrine. The purpose of the present investigation was to determine whether stimulation of carotid chemoreceptors by epinephrine is a direct effect or secondary to epinephrine-induced increases in arterial plasma [K+] and whole body CO2 production (VCO2). Chemoreceptor discharge was recorded from single fiber preparations of the carotid sinus nerves in anesthetized cats ventilated to a constant arterial PCO2 (PaCO2). Infusion of epinephrine (1 microgram.kg-1 x min-1) caused arterial [K+] to increase from a mean of 2.7 to 3.8 mM. VCO2 increased so that ventilation had to be increased by 60% to maintain PaCO2 constant. Mean chemoreceptor discharge increased by 50%, but this was no greater than would be predicted on the basis of the increases in arterial [K+] and VCO2. In a further group of experiments epinephrine was infused at 0.1 microgram.kg-1 x min-1 and produced no significant increase in chemoreceptor firing. These experiments provide no evidence for epinephrine having a direct effect on the carotid chemoreceptor.


1982 ◽  
Vol 242 (2) ◽  
pp. H220-H226
Author(s):  
F. Karim ◽  
D. U. Mackay ◽  
C. T. Kappagoda

Stimulation of the atrial receptors results in an increase in renal blood flow. The present investigation was undertaken to determine whether this response was modulated by the input from the baroceptors in the carotid sinus. The experiments were performed on dogs anesthetized with chloralose. The systemic arterial pressure was held constant. The carotid sinuses were perfused at 62 +/- 1.3, 95 +/- 2.7, and 145 +/- 8.3 mmHg. The atrial receptors were stimulated by distension of small balloons positioned at the left pulmonary vein-atrial junctions and the left atrial appendage. At a carotid sinus pressure of 62 +/- 1.3 mmHg, the blood flow increased from 182 +/- 8.5 to 199 +/- 8.9 ml . min-1 . 100 g-1 renal mass. At a carotid sinus pressure of 95 +/- 2.7 mmHg, the blood flow increased from 202 +/- 9.6 to 209 +/- 10.4 ml . min-1 . 100 g-1 renal mass. At a carotid sinus pressure of 145 +/- 8.3 mmHg, the blood flow increased from 237 +/- 13.0 to 239 +/- 12.5 ml . min-1 . 100 g-1 renal mass. The first two responses alone were statistically significant. The response at a carotid sinus pressure of 62 +/- 1.3 mmHg was abolished by cutting or cooling the cervical vagi to 8--10 degrees C. It is concluded that stimulation of the left atrial receptors produces a reflex increase in blood flow to the kidney, and this response is modulated by the input from the carotid sinus baroceptors.


1985 ◽  
Vol 248 (5) ◽  
pp. H631-H636 ◽  
Author(s):  
K. K. Teo ◽  
G. C. Man ◽  
C. T. Kappagoda

This study was undertaken to determine the influence of 1) the left atrial receptors (LA) on the ability of the carotid sinus baroreceptors (CS) to regulate heart rate and 2) the CS on the reflex increase in heart rate mediated by the LA. The LA were stimulated by stretching the pulmonary vein-atrial junctions in dogs anesthetized with alpha-chloralose. Aortic pressure was controlled, and the pressure in the CS was regulated. Stimulus-response curves were obtained relating heart rate to pressures in the CS, in the control state, and during stimulation of LA (6 dogs). Factorial analysis revealed that LA exerted a significant influence on heart rate (P less than 0.01). Next the CS pressure was set at mid, low, and high levels and the LA stimulated. It was found that the effect on heart rate was greatest at the mid setting (+19.3 +/- 2.9 beats/min) and least at the low setting of the pressure in the CS (+0.9 +/- 0.5, 11 dogs). Sympathetic blockade attenuated significantly the response in the mid setting of the CS pressure and left intact the response at the high setting of the pressure in the CS. It is concluded that there is a significant interaction between these two reflexes.


Sign in / Sign up

Export Citation Format

Share Document