Role of the carotid sinus pressure receptors in reflex regulation of hemodynamic changes in unanesthetized animals exposed to transverse accelerations

1967 ◽  
Vol 64 (6) ◽  
pp. 1285-1287
Author(s):  
E. B. Shul'zhenko
1976 ◽  
Vol 230 (1) ◽  
pp. 19-24 ◽  
Author(s):  
G Mancia ◽  
JT Shepherd ◽  
DE Donald

Interactions among vascular reflexes evoked from carotid sinuses, carotid bodies, and cardiopulmonary region were examined in anesthetized, atropinized, and respired dogs with aortic nerves cut. The carotid sinuses were perfused at 220, 150, and 40-50 mmHg; the chemoreceptors were stimulated by perfusion with hypoxic hypercapnic blood. Cardiopulmonary vasomotor inhibition was interrupted by vagal cold block. Measurements were made of arterial blood pressure and of kidney and hindlimb vascular resistance. At sinus pressures less than 170-160 mmHg, cardiopulmonary vasomotor inhibition increased with increase in blood volume. At high sinus pressure, interruption of this augmented cardiopulmonary inhibition was as ineffective in changing vascular resistance as interruption of the lesser inhibition present during normovolemia. Chemoreceptor stimulation increased the response to vagal block at intermediate but not at high or low sinus pressure. The studies demonstrate the dominant role of the carotid sinus reflex when the three systems interact and the ineffectiveness of chemoreceptor stimulation when carotid or cardiopulmonary inhibition is maximal.


1981 ◽  
Vol 241 (6) ◽  
pp. H802-H806 ◽  
Author(s):  
D. L. Kunze

The carotid baroreceptor depressor reflex of the chloralose-anesthetized cat was examined to determine the role of the prevailing carotid pressure in determining the threshold, gain, and range of operation of the reflex response. After the pressure of an isolated perfused carotid sinus was held at 80 mmHg for 20 min the threshold pressure necessary to elicit the reflex systemic blood pressure response was 78 +/- 2.9 (SE) mmHg (n = 5). When carotid pressure was maintained for 20 min at 120 and 160 mmHg the threshold rose to 113 +/- 2.9 and 126 +/- 3.0 mmHg, respectively. The resetting of the threshold to a stable value upon elevating or reducing carotid sinus pressure was accomplished within 15—;20 min. The entire range of operation of the reflex response was shifted to higher carotid pressures as the holding pressure was elevated. The midrange gain of the response was unchanged at the three holding pressures tested. These findings indicate that the carotid baroreceptor reflex need not operate over a fixed range but that the range may be rapidly adjustable to the prevailing pressure. When arterial pressure is sustained at a level that is elevated or depressed from normal the carotid baroreceptor reflex acutely resets to operate in the range of the prevailing pressure with a threshold that has moved toward the prevailing pressure.


1997 ◽  
Vol 273 (4) ◽  
pp. H1713-H1718
Author(s):  
F. Karim ◽  
S. M. Poucher

The role of β- and α-adrenoceptors in the total vascular capacitance responses to changing pressure in vascularly isolated carotid sinuses of anesthetized and atropinized dogs was investigated. A change in vascular capacitance was determined by measuring the shift of blood in and out of a reservoir that was connected to the aorta and maintained at a constant pressure. Changes in carotid sinus pressure from 135 to 57 mmHg and back to 137 mmHg resulted in a rapid vascular capacitance response of ∼30 ml in the absence of adrenoceptor antagonists. Administration of a β2-adrenoceptor antagonist (ICI-118551) caused a significant enhancement of the capacitance responses to similar decreases and increases in carotid sinus pressure (∼130%). Administration of a β1-adrenoceptor antagonist (CGP-20712A) did not cause any further enhancement of the responses. However, an α-blocker (phentolamine) reduced the responses by 75%. The results suggest that in the presence of a β2-adrenoceptor antagonist vascular capacitance responses to loading and unloading of baroreceptors are greatly enhanced and that patients suffering from orthostatic syncope may benefit from this kind of drug.


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