Cardioinhibitory actions of clonidine assessed by cardiac vagal motoneuron recordings

Toader, Emil; Cividjian, Andrei; Rentero, N.; McAllen, Robin M.; Quintin, Luc

doi:10.1097/hjh.0b013e3282fd10e0

Cited by 21 publications

(38 citation statements)

References 49 publications

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“…As reported, clonidine (100 g/kg) decreased arterial pressure and HR, while increasing CVM activity (Fig. 3C) and the slope of its response to SBP (53). The following results are novel.…”

Section: Ratssupporting

confidence: 62%

“…It is established that clonidine increases the gain of the cardiac baroreflex in humans (37,46,51) and other species (28,53). This is attributable at least partly to increased sensitivity of the arterial stretch receptors themselves (1,28,30), to an action in the nucleus tractus solitarius (44,49), and probably also to increased excitability of CVM, whose firing pattern after clonidine changes to include many short bursts (doublet and triplet spikes) (53).…”

Section: Clonidine and The Cardiac Baroreflexmentioning

confidence: 99%

“…Clonidine 100 g/kg iv (50 g/ml in saline; Sigma, St Louis, MO) was infused over ϳ10 min. This dose has been shown to increase CVM activity and alter its firing pattern (53). For compari- Typical traces for SBP (mmHg) and R-R interval (ms) in 1 healthy resting supine volunteer before (A) and 120 min after (B) administration of 6 g/kg po clonidine.…”

Section: Ratsmentioning

confidence: 99%

“…Experiments were approved by the Rhône-Alpes Committee for the Care of Animals and were performed on Sprague-Dawley male rats, as reported earlier (53) (325-400 g body wt; Harlan, Gannat, France) according to National Institutes of Health guidelines (33a). Data from CVM recordings and HR obtained in the course of a previous study (53) were reanalyzed. The methods were described in the earlier publication (53) but will be outlined here.…”

Section: Ratsmentioning

confidence: 99%

“…Using data previously collected from healthy human volunteers (37), sBRS (13) and xBRS (56) algorithms were used to test this prediction. To generalize the findings in a second species and to pursue the mechanisms responsible, data on HR and the activity of cardiac vagal motoneurons (CVM) (32,40,53) were taken from a published study on anesthetized rats (53), reanalyzed, and supplemented with further experiments. These steps allowed the central and efferent components of the reflex pathway to be studied independently of each other, clarifying the site and mode of action of clonidine on cardiac baroreflex delay.…”

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confidence: 99%

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Effect of clonidine on cardiac baroreflex delay in humans and rats

Cividjian

Toader

Wesseling

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Cividjian A, Toader E, Wesseling KH, Karemaker JM, McAllen R, Quintin L. Effect of clonidine on cardiac baroreflex delay in humans and rats. Am J Physiol Regul Integr Comp Physiol 300: R949-R957, 2011. First published January 26, 2011 doi:10.1152/ajpregu.00438.2010The delay between rising systolic blood pressure (SBP) and baroreflex bradycardia has been found to increase when vagal tone is low. The ␣2-agonist clonidine increases cardiac vagal tone, and this study tested how it affects . In eight conscious supine human volunteers clonidine (6 g/kg po) reduced , assessed both by cross correlation baroreflex sensitivity and sequence methods (both P Ͻ 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 (P Ͻ 0.05) after clonidine (100 g/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 ϭ 5, P Ͻ 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 not by changing central or efferent latencies but simply by slowing the heart. sequences; lag; latency; cardiac vagal motoneurons; ␣ 2-agonist THE GAIN OF THE ARTERIAL baroreceptor-heart rate reflex (cardiac baroreflex) has been calculated from the relationship between spontaneous (10, 13) or drug-induced (47) increases in systolic blood pressure (SBP) and the accompanying decrease in heart rate (HR). In humans, the best correlations were initially obtained by relating cardiac intervals to the preceding SBP (delay ϭ 1 beat) (47), although later studies (14, 38) found a delay of 0 beat was appropriate in subjects with lower initial HRs. In unanesthetized rats, delays of between 2 and 14 beats gave the best correlation for spontaneous baroreflex measurements (35); the best fit for tachycardic responses was 2 to 3 beats longer than that for bradycardic responses (35). The sequence technique of baroreflex sensitivity (sBRS) (13) traditionally uses a constant delay ϭ 1 beat to measure spontaneous baroreflex slope in humans, although the method may be applied using delays of any whole number of beats. This approach has been expanded to give a near-continuous assessment of the slope of the cardiac baroreflex [time-domain cross-correlation BRS (xBRS)] (56). The algorithm of xBRS (56) adjusts in seconds...

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“…As reported, clonidine (100 g/kg) decreased arterial pressure and HR, while increasing CVM activity (Fig. 3C) and the slope of its response to SBP (53). The following results are novel.…”

Section: Ratssupporting

confidence: 62%

Section: Clonidine and The Cardiac Baroreflexmentioning

confidence: 99%

Section: Ratsmentioning

confidence: 99%

Section: Ratsmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of clonidine on cardiac baroreflex delay in humans and rats

Cividjian

Toader

Wesseling

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Dexmédétomidine et clonidine : revue de leurs propriétés pharmacodynamiques en vue de définir la place des agonistes alpha-2 adrénergiques dans la sédation en réanimation

Pichot

Longrois

Ghignone

et al. 2012

Annales Françaises d'Anesthésie et de Réanimation

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Information domain analysis of the spontaneous baroreflex during pharmacological challenges

Porta

Castiglioni

Rienzo

et al. 2013

Autonomic Neuroscience

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The information carried by heart period (HP) given systolic arterial pressure (SAP) changes was assessed to characterize spontaneous baroreflex (i.e. the relation linking SAP variability to HP variability): the larger the information carried by HP given SAP changes, the greater the unpredictability of HP given SAP variations, the smaller the strength of the causal coupling from SAP series to HP series. It was typified according to two parameters: i) the information carried by HP given SAP changes within the same heart cycle (i.e. 0-step-ahead information) describing immediate effects of SAP variations on HP; ii) the rate of increase of the information carried by HP given SAP changes as a function of the temporal distance, k, between the conditioning SAP pattern and future HP value (i.e. the rate of increase of k-step-ahead information with k) describing short-term effects of SAP modifications on HP. Both parameters were found under vagal control. Indeed, i) 0-step-ahead information suggested that HP and SAP variabilities were significantly coupled from SAP to HP at baseline and after the reduction of the inhibitory effect of sympathetic control on vagal influences performed through the administration of propranolol or clonidine; and ii) during vagal blockade induced by atropine or combined vagal and sympathetic blockade induced by the administration of propranolol after atropine k-step-ahead information reached a level incompatible with coupled HP and SAP dynamics regardless of k. In addition, it was found that the 0-step-ahead information at baseline and after propranolol and the rate of increase of k-step-ahead information with k at baseline could be exclusively explained in terms of linear HP–SAP interactions. Conversely, the same parameters after clonidine suggested the raise of nonlinear mechanisms probably unveiled by the central sympathetic blockade. Comparison with more traditional parameters describing the HP–SAP variability relation such as baroreflex sensitivity and squared HP–SAP coherence confirmed the complementary value of the proposed information domain analysis.

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Cardioinhibitory actions of clonidine assessed by cardiac vagal motoneuron recordings

Abstract: Such grouped patterns are known to enhance neurotransmitter release. Therefore, these data provide a new mechanism by which clonidine can further potentiate parasympathetic actions on the heart.

Cited by 21 publications

References 49 publications

Effect of clonidine on cardiac baroreflex delay in humans and rats

Effect of clonidine on cardiac baroreflex delay in humans and rats

Dexmédétomidine et clonidine : revue de leurs propriétés pharmacodynamiques en vue de définir la place des agonistes alpha-2 adrénergiques dans la sédation en réanimation

Information domain analysis of the spontaneous baroreflex during pharmacological challenges

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