Effect of clonidine on cardiac baroreflex delay in humans and rats

The delay τ between rising systolic blood pressure (SBP) and baroreflex bradycardia has been found to increase when vagal tone is low. The α(2)-agonist clonidine increases cardiac vagal tone, and this study tested how it affects τ. In eight conscious supine human volunteers clonidine (6 μg/kg po) re...

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Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2011-04, Vol.300 (4), p.R949-R957
Main Authors: Cividjian, Andrei, Toader, Emil, Wesseling, Karel H, Karemaker, John M, McAllen, Robin, Quintin, Luc
Format: Article
Language:English
Subjects:
Adrenergic alpha-2 Receptor Agonists - pharmacology
Adult
Animals
Baroreflex - drug effects
Baroreflex - physiology
Blood pressure
Blood Pressure - drug effects
Blood Pressure - physiology
Catheters
Clonidine - pharmacology
Correlation analysis
Effects
Electric Stimulation
Electrocardiography
Heart - drug effects
Heart - innervation
Heart - physiology
Heart rate
Heart Rate - drug effects
Heart Rate - physiology
Humans
Male
Middle Aged
Models, Animal
Motor Neurons - drug effects
Motor Neurons - physiology
Rats
Rats, Sprague-Dawley
Rodents
Stroke Volume - drug effects
Stroke Volume - physiology
Time Factors
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Summary:The delay τ between rising systolic blood pressure (SBP) and baroreflex bradycardia has been found to increase when vagal tone is low. The α(2)-agonist clonidine increases cardiac vagal tone, and this study tested how it affects τ. In eight conscious supine human volunteers clonidine (6 μg/kg po) reduced τ, assessed both by cross correlation baroreflex sensitivity and sequence methods (both P < 0.05). Experiments on urethane-anaesthetized rats reproduced the phenomenon and investigated the underlying mechanism. Heart rate (HR) responses to increasing SBP produced with an arterial balloon catheter showed reduced τ (P < 0.05) after clonidine (100 μg/kg iv). The central latency of the reflex was unaltered, however, as shown by the unchanged timing with which antidromically identified cardiac vagal motoneurons (CVM) responded to the arterial pulse. Testing the latency of the HR response to brief electrical stimuli to the right vagus showed that this was also unchanged by clonidine. Nevertheless, vagal stimuli delivered at a fixed time in the cardiac cycle (triggered from the ECG R-wave) slowed HR with a 1-beat delay in the baseline state but a 0-beat delay after clonidine (n = 5, P < 0.05). This was because clonidine lengthened the diastolic period, allowing the vagal volleys to arrive at the heart just in time to postpone the next beat. Calculations indicate that naturally generated CVM volleys in both humans and rats arrive around this critical time. Clonidine thus reduces τ not by changing central or efferent latencies but simply by slowing the heart.
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00438.2010