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Responses to stimulation of coronary and carotid baroreceptors and the coronary chemoreflex at different ventricular distending pressures in anaesthetised dogs

Published online by Cambridge University Press:  31 July 2001

C. I. Wright
Affiliation:
Institute of Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK
M. J. Drinkhill
Affiliation:
Institute of Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK
R. Hainsworth
Affiliation:
Institute of Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK
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Abstract

Stimulation of left ventricular mechanoreceptors was believed not only to exert important effects on the circulation, but also to influence the responses to baroreceptor reflexes. However, most previous work is flawed due to inadequate localisation of stimuli to specific reflexogenic areas. In this study, we applied a discrete stimulus to left ventricular mechanoreceptors to examine other reflexes known to effect the circulation. Dogs were anaesthetised, artificially ventilated and a cardiopulmonary bypass established. The pressure distending the left ventricle was controlled through an apical cannula with the aortic valve obstructed by a balloon. Changes in ventricular systolic and end-diastolic pressure had only a small effect on vascular resistance, assessed as perfusion pressure in the systemic circulation (flow constant). Responses to changes in carotid or coronary pressure or to stimulation of chemosensitive afferents by injecting veratridine into the coronary circulation were always much larger. Responses to stimulation of these reflexes were little affected by the level of stimulus to the ventricular receptors. These experiments confirm that responses to stimulation of ventricular mechanoreceptors are very small and show that they remain small at different levels of input to other baroreceptive regions. There was no evidence of interaction between ventricular mechanoreceptor reflexes and carotid or coronary baroreceptors or ventricular chemosensitive reflexes. Experimental Physiology (2001) 86.3, 381-390.

Type
Research Article
Copyright
© The Physiological Society 2001

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