Increased activity of carotid sinus baroreceptors by sympathetic stimulation and norepinephrine

1981 ◽  
Vol 240 (4) ◽  
pp. H650-H658 ◽  
Author(s):  
E. Tomomatsu ◽  
K. Nishi
Keyword(s):  
Carotid Sinus ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Nerve Endings ◽  
Discharge Frequency ◽  
Sympathetic Stimulation ◽  
High Concentration ◽  
Excitatory Effect ◽  
Pressure Step ◽  
Stimulation Of

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.

Sympathetic Stimulation and Otic Blood Flow

1974 ◽  
Vol 83 (1) ◽  
pp. 84-91 ◽  
Author(s):  
N. W. Todd ◽  
J. E. Dennard ◽  
A. A. Clairmont ◽  
R. T. Jackson
Keyword(s):  
Blood Flow ◽  
Temporal Bone ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Bone Blood Flow ◽  
Sympathetic Stimulation ◽  
Nasal Tissue ◽  
Norepinephrine Infusion ◽  
Cervical Sympathetic ◽  
Cervical Ganglia

The radioactive microsphere technique was used in dogs to assess the effect of sympathetic stimulation on temporal bone blood flow. The stellate, caudal cervical and superior cervical ganglia, and the vertebral and cervical sympathetic nerves were stimulated. In a large majority of the animals, stimulation had no effect on temporal bone blood flow although nasal tissue was greatly affected. In a minority of animals, a small effect was seen in temporal bone tissue. Similarly, norepinephrine infusion usually did not produce evidence of reduced blood flow in the temporal bone. It was concluded that the sympathetic innervation of otic blood vessels was not capable of controlling otic blood flow, only modulating it. A sympathetic vasospasm does not seem possible. Mention is made of the dual sympathetic innervation of the cochlea described by Spoendlin and Ross. The possible mediation of sympathetic effects in the cochlea by cyclic AMP is suggested.

Autonomic Balance in Cardiac Control

1958 ◽  
Vol 192 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Heart Rate ◽  
Mechanical Performance ◽  
Stimulus Frequency ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Sympathetic Stimulation ◽  
Vagus Nerves ◽  
Ventricular Performance ◽  
Anesthetized Dogs ◽  
Stimulation Of

Stimulation of the sympathetic nerves to the heart in anesthetized dogs produced tachycardia and changes in left ventricular performance, including alterations in both pressures and dimensions. Stimulation of the vagus nerves in dogs predominately induced a bradycardia. When the heart rate was controlled by an artificial pacemaker, sympathetic stimulation produced changes in ventricular performance. By adjustments in stimulus frequency, the effects of vagal and sympathetic stimulation on heart rate could be balanced, but complete cancellation of effects was impossible because the vagus had a more powerful effect on heart rate and the sympathetic nerves had a greater influence on mechanical performance.

scholarly journals The sympathetic nervous system in white adipose tissue regulation

2001 ◽  
Vol 60 (3) ◽  
pp. 357-364 ◽  
Author(s):  
D. Vernon Rayner
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Sympathetic Innervation ◽  
Sympathetic System ◽  
Adrenergic Blockade ◽  
Sympathetic Stimulation ◽  
White Fat ◽  
Leptin System ◽  
Stimulation Of

Sympathetic stimulation has long been recognized to mobilise fatty acids from white adipose tissue. However, it is now apparent that adipose tissue is not only concerned with energy storage as fat, but is a major endocrine and secretory organ. This change has resulted from the identification of leptin as a hormone of energy balance secreted by white adipose tissue. The sympathetic system is a key regulator of leptin production in white fat. Sympathomimetic amines, cold exposure or fasting (which lead to sympathetic stimulation of white fat), decrease ob gene expression in the tissue and leptin production. On the other hand, sympathetic blockade often increases circulating leptin and ob gene expression, and it is postulated that the sympathetic system has a tonic inhibitory action on leptin synthesis. In rodents this action is through stimulation of b3-adrenoceptors. The adrenal medulla (as opposed to the direct sympathetic innervation) has been thought to play only a minor role in the catecholaminergic regulation of white adipose tissue. However, in rodents responses of the leptin system to adrenergic blockade vary with the method used. Changes in leptin and ob gene expression are considerably less using methods of blockade that only effect the terminal adrenergic innervation, rather than medullary secretions as well. Stimulation of the leptin system increases sympathetic activity and hence metabolic activity in many tissues. As well as leptin, other (but not all) secretions from white adipose tissue are subject to sympathetic regulation. In obesity the sympathetic sensitivity of adipose tissue is reduced and this factor may underlie the dysregulation of leptin production and other adipose tissue secretions.

Reflex modulation of carotid sinus baroreceptor activity in the dog

1983 ◽  
Vol 244 (3) ◽  
pp. H437-H443 ◽  
Author(s):  
R. B. Felder ◽  
C. M. Heesch ◽  
M. D. Thames
Keyword(s):  
Arterial Pressure ◽  
Inferior Vena ◽  
Carotid Sinus ◽  
Sympathetic Nerves ◽  
Reflex Modulation ◽  
Inferior Vena Caval ◽  
Anesthetized Dogs ◽  
Induced Changes ◽  
Sympathetic Discharge ◽  
Stimulation Of

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.

Attenuation of reactive and active hyperemia by sympathetic stimulation in dog gracilis muscle

1986 ◽  
Vol 251 (6) ◽  
pp. H1183-H1187 ◽  
Author(s):  
R. E. Klabunde
Keyword(s):  
Reactive Hyperemia ◽  
Low Frequency ◽  
Arterial Occlusion ◽  
Sympathetic Nerves ◽  
Sympathetic Stimulation ◽  
Tetanic Contraction ◽  
Contraction Duration ◽  
Muscle Ischemia ◽  
Frequency Of Stimulation ◽  
Stimulation Of

The effects of sympathetic stimulation (SS) on reactive hyperemia (RH) and active hyperemia (AH) were evaluated in dog gracilis muscles. Sympathetic nerves to the muscle vasculature were activated by electrical stimulation of the obturator nerve during neuromuscular blockade. The frequency of stimulation was adjusted to decrease control conductance by 50%. RH responses to 1 and 5 min of arterial occlusion and AH after 1, 4, 7, and 10 s of tetanic contraction (direct muscle stimulation) at 30% maximal tensions were recorded in the absence and presence of SS. RH peak conductance (Cp), recovery half-time (T0.5), and excess flow (EQ) were significantly attenuated by SS at both occlusion durations. The change in conductance (delta C) during RH was not altered by SS, since the absolute reductions in control and peak conductances were not different. The Cp of AH was reduced at each contraction duration while the delta C was reduced only with 1-s contractions. The T0.5 and EQ of AH were not affected by SS. The data demonstrate that low frequency SS limits the degree of vasodilation associated with both muscle ischemia and tetanic contraction. Furthermore, the more pronounced effects of SS on RH suggest that there is greater inhibition of sympathetic vasoconstrictor influences associated with muscle contraction than muscle ischemia possibly due to the production of a substance during contraction, but not ischemia, that antagonizes sympathetic vasoconstrictor mechanisms.

Control of movements of the stomach and spiral intestine of Raja and Scyliorhinus

1983 ◽  
Vol 63 (3) ◽  
pp. 557-574 ◽  
Author(s):  
J. Z. Young
Keyword(s):  
Vagus Nerve ◽  
Sympathetic Nerves ◽  
Slight Reduction ◽  
High Concentration ◽  
Spiral Intestine ◽  
Cardiac Stomach ◽  
Excitatory Response ◽  
Acetyl Choline ◽  
Spontaneous Contractions ◽  
Stimulation Of

The extrinsic nerves of the stomach of dogfish and skates regulate the frequency and amplitude of contraction by inhibition followed by rebounds. By contrast the nerves of the spiral intestine are excitatory.Stimulation of the vagus nerve of the ray produced slight reduction in the amplitude of spontaneous contractions of the cardiac stomach. Much greater inhibition was produced by stimulation of the sympathetic nerves and was followed by large rebound contractions. These effects were imitated by adrenalin and serotonin which altered the frequency and amplitude of contraction in various ways. These actions were not blocked by either propranalol (1–5 × 10−5 M) or phentolamine (2 × 10−5 M) and indeed were often increased. The excitatory response to adrenalin was not blocked by TTX even after this had blocked the response to the nerve. Responses both to the nerve and adrenaline were blocked by trazodone. Acetyl choline caused some contraction of the stomach but only at high concentration.Muscles of the spiral intestine of Raja or Scyliorhinus were activated by stimulation of their sympathetic nerves and by adrenalin. These responses were not blocked by phentolamine and only reduced by propranalol They were blocked by trazodone. The response to adrenalin continued after the nerve was blocked by TTX. Acetyl choline had very little effect on the spiral intestine.The striking differences between the responses of the stomach and intestine are probably related to the fact that the plexus in the latter contains no nerve cells. The neurons in the stomach are therefore presumbly connected with the inhibition and large rebound contractions.

Baroreflex Sensitivity Assessment – Latest Advances and Strategies

2011 ◽  
Vol 7 (2) ◽  
pp. 89 ◽  
Author(s):  
Maria Teresa La Rovere ◽  
Roberto Maestri ◽  
Gian Domenico Pinna ◽  
◽  
◽  
...  
Keyword(s):  
Baroreflex Sensitivity ◽  
Carotid Sinus ◽  
Lower Blood Pressure ◽  
Vasomotor Tone ◽  
Sensitivity Assessment ◽  
Lower Blood ◽  
Prognostic Implications ◽  
Novel Therapeutic Strategies ◽  
Sympathetic Vasomotor Tone ◽  
Stimulation Of

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.

Electrical stimulation of the carotid sinus lowers arterial pressure and improves heart rate variability in l-NAME hypertensive conscious rats

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 ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Conscious Rats ◽  
Stimulation Of

scholarly journals Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation

2008 ◽  
Vol 295 (2) ◽  
pp. H691-H698 ◽  
Author(s):  
Alex Y. Tan ◽  
Shengmei Zhou ◽  
Byung Chun Jung ◽  
Masahiro Ogawa ◽  
Lan S. Chen ◽  
...  
Keyword(s):  
Pulmonary Vein ◽  
Sinus Node ◽  
Periodic Acid ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Atrial Arrhythmias ◽  
Periodic Acid Schiff ◽  
Stellate Ganglia ◽  
Ectopic Beats

The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein ( n = 11), right atrium ( n = 5), left atrium ( n = 2), and the vein of Marshall ( n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells ( P < 0.05) and sympathetic nerves ( P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

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