Blood pressure and heart rate changes during physical activity upon heart rate feedback-controlled electrical carotid sinus nerve stimulation

1989 ◽  
Vol 22 (3) ◽  
pp. 389-392 ◽  
Author(s):  
Tim K. Peters ◽  
H.-E. Koralewski ◽  
E. Zerbst
1992 ◽  
Vol 73 (5) ◽  
pp. 2166-2171 ◽  
Author(s):  
J. E. Melton ◽  
Q. P. Yu ◽  
J. A. Neubauer ◽  
N. H. Edelman

This study examines the effect of progressive isocapnic CO hypoxemia on respiratory afterdischarge and the phrenic neurogram response to supramaximal carotid sinus nerve (CSN) stimulation. Twelve anesthetized, vagotomized, peripherally chemodenervated, ventilated cats with blood pressure controlled were studied. During isocapnic hypoxemia, the amplitude of the phrenic neurogram was progressively depressed. In contrast, the increase in peak phrenic amplitude produced by CSN stimulation was unchanged, suggesting that the central respiratory response to CSN stimulation is unaffected by progressive hypoxemia. The time constant of respiratory afterdischarge (tau) was calculated from best-fit plots of phrenic amplitude vs. time after cessation of CSN stimulation. Under control conditions the value of tau was 57.7 +/- 3 (SE) s (n = 12). During progressive isocapnic hypoxemia, tau decreased as a linear function of arterial O2 content (CaO2) such that a 40% reduction of CaO2 resulted in a 48% reduction in tau. This reduction of respiratory afterdischarge may contribute to the genesis of periodic breathing during hypoxia.


1980 ◽  
Vol 58 (1) ◽  
pp. 7-13 ◽  
Author(s):  
J. D. Marker ◽  
T. S. Miles ◽  
G. C. Scroop

1. The effects of vascular infusions of acetylcholine, angiotensin II, noradrenaline and prostaglandin F2α on the baroreceptor reflex were studied in the anaesthetized greyhound. 2. Vertebral artery infusions of low doses of angiotensin II, but not of acetylcholine or prostaglandin F2α, resulted in a significant reduction in the depressor response to carotid sinus nerve stimulation. 3. The increases in blood pressure and heart rate in response to bilateral carotid artery occlusion were not significantly changed during vertebral artery infusions of acetylcholine, angiotensin II or prostaglandin F2α. 4. The increases in blood pressure in response to intravenous infusions of noradrenaline were significantly enhanced during vertebral artery infusions of acetylcholine and angiotensin II, but not of prostaglandin F2α. The bradycardia during noradrenaline infusions was significantly enhanced by angiotensin II alone. 5. The depressor response to carotid sinus nerve stimulation was significantly reduced during intravenous infusions of both noradrenaline and angiotensin II. 6. It is considered that although angiotensin II can be shown to have a specific central action to attenuate the response to carotid sinus nerve stimulation, the role of this action in the complete baroreceptor reflex is unproven.


Hypertension ◽  
2018 ◽  
Vol 72 (Suppl_1) ◽  
Author(s):  
Aline B Ribeiro ◽  
Patricia G Fernandes ◽  
Fernanda Brognara ◽  
Jaci A Castania ◽  
Carlos A Silva ◽  
...  

2008 ◽  
Vol 47 (4) ◽  
pp. 402-408 ◽  
Author(s):  
Alison M. McManus ◽  
Rich S.W. Masters ◽  
Raija M.T. Laukkanen ◽  
Clare C.W. Yu ◽  
Cindy H.P. Sit ◽  
...  

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