Electrical Stimulation of Vascular Autonomic Nerves: Effects on Heart Rate, Blood Pressure, and Arrhythmias

2015 ◽  
Vol 38 (7) ◽  
pp. 825-830 ◽  
Author(s):  
JIAN SUN ◽  
BENJAMIN J. SCHERLAG ◽  
BO HE ◽  
XIAOHUA SHEN ◽  
MEI GAO ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Autonomic Nerves ◽  
Stimulation Of

Axons of passage may be responsible for fastigial nucleus pressor response

1989 ◽  
Vol 257 (6) ◽  
pp. R1436-R1440
Author(s):  
R. T. Henry ◽  
J. D. Connor
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Kainic Acid ◽  
Pulse Width ◽  
Pressor Response ◽  
Fastigial Nucleus ◽  
Postural Asymmetry ◽  
Bilateral Destruction ◽  
Stimulation Of

Bilateral destruction of perikarya in the fastigial nucleus (FN) of the rat with the cytotoxic agent kainic acid (0.5 mg) did not alter the blood pressure (BP) increases observed during monopolar electrical stimulation (100 microA, 50 Hz, 0.5-ms pulse width) of this region. BP increases in control animals were 30 +/- 8 mm Hg, whereas BP increased 30 +/- 7 mmHg in kainic acid-lesioned rats. Furthermore, picrotoxin (100 ng) and muscimol (25 ng) microinjected unilaterally into the FN of conscious, unrestrained rats produced postural asymmetry but no change in BP or heart rate. These data suggest that the FN pressor response may be due, at least in part, to stimulation of axons of passage.

scholarly journals Electrical stimulation of the midbrain increases heart rate and arterial blood pressure in awake humans

2002 ◽  
Vol 539 (2) ◽  
pp. 615-621 ◽  
Author(s):  
Judith M. Thornton ◽  
Tipu Aziz ◽  
David Schlugman ◽  
David J. Paterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Stimulation Of

Effects of electrical stimulation of the pontine A5 cell group on blood pressure and heart rate in the rabbit

1986 ◽  
Vol 379 (1) ◽  
pp. 10-23 ◽  
Author(s):  
Michael L. Woodruff ◽  
Ronald H. Baisden ◽  
Dennis L. Whittington
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Cell Group ◽  
Stimulation Of

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

Vagal function impairment after exercise training

1992 ◽  
Vol 72 (5) ◽  
pp. 1749-1753 ◽  
Author(s):  
C. E. Negrao ◽  
E. D. Moreira ◽  
M. C. Santos ◽  
V. M. Farah ◽  
E. M. Krieger
Keyword(s):  
Heart Rate ◽  
Electrical Stimulation ◽  
Exercise Training ◽  
Marked Reduction ◽  
Resting Heart Rate ◽  
Pacemaker Cells ◽  
Function Impairment ◽  
Stimulation Of ◽  
Vagal Function

The present investigation was undertaken to evaluate the vagal function of trained (T) and sedentary (S) rats by use of different approaches in the same animal. After 13 wk of exercise training (treadmill for 1 h 5 times/wk at 26.8 m/min and 15% grade), T rats had a resting heart rate (HR) slightly but significantly lower than S rats (299 +/- 3 vs. 308 +/- 3 beats/min). T rats had marked reduction of the intrinsic HR (329 +/- 4 vs. 369 +/- 5 beats/min) after blockade by methylatropine and propranolol. They also exhibited depressed vagal and sympathetic tonus. Baroreflex bradycardia (phenylephrine injections) was reduced, bradycardic responses produced by electrical stimulation of the vagus were depressed, and responses to methacholine injection were decreased in T rats. Therefore several evidences of vagal function impairment were observed in T rats. The resting bradycardia after exercise training is more likely to be dependent on alterations of the pacemaker cells, inasmuch as the intrinsic HR was markedly reduced.

Interaction of aortic and carotid sinus baroreceptors: effect of activation times

1975 ◽  
Vol 228 (1) ◽  
pp. 238-243 ◽  
Author(s):  
PG Katona ◽  
KS Tan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Carotid Sinus ◽  
Relative Timing ◽  
Relative Delay ◽  
Activation Times

Changes in pulse-wave velocity were simulated by changing the relative timing between aortic and carotid sinus barorecptor activity in anesthetized rabbits and dogs. In the rabbit, electrical stimulation was used to vary the timing; in the dog, it was also varied by perfusing the carotid sinuses with externally generated pressure pulses that could be triggered in any portion of the cardiac cycle. Changing the relative delay between aortic and carotid sinsus nerve stimulation did not result in variations of blood pressure or heart rate in the rabbit. Varing the time of electrical stimulation of the carotid sinus nerve caused at most 5 mmHg change of blood pressure in the dog. Delay-related heart-rate changes could be usually observed only when the stimulus consisted of short, high-intensity bursts. When the carotid sinus was externally perfused with pulses of pressure, only one out of five dogs showed delay-related variations in blood pressure (3mmHg) and heart rate (6 beats/min). It is concluded that variations in pulse-wave velocity are unlikely to play a significant role in acute cardiovascular control.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

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