The haemodynamic and hormonal responses after clonidine occur independently of sedation in essential hypertension.

Kooner, JS; Peart, W. S.; Mathias, C. J.

doi:10.1111/j.1365-2125.1989.tb05423.x

Cited by 10 publications

(6 citation statements)

References 20 publications

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“…The significant reduction of systolic blood pressure by clonidine is consistent with previous reports (e.g. Kooner et al, 1989), and is compatible with an interaction of clonidine with central and/or peripheral a2adrenoceptors (Kobinger, 1978).…”

Section: Discussionsupporting

confidence: 92%

“…The attenuation of this effect by yohimbine is consistent with an involvement of central a2-adrenoceptors in clonidine's sedative action (Kooner et al, 1989).…”

Section: Discussionsupporting

confidence: 74%

“…The reduction of subjectively-rated 'alertness' by clonidine is consistent with its known sedative properties (Kooner et al, 1989). The attenuation of this effect by yohimbine is consistent with an involvement of central a2-adrenoceptors in clonidine's sedative action (Kooner et al, 1989).…”

Section: Discussionsupporting

confidence: 59%

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Effects of clonidine and yohimbine on the pupillary light reflex and carbachol‐evoked sweating in healthy volunteers.

Morley

Bradshaw

Szabadi

1991

Brit J Clinical Pharma

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The effects of single doses of clonidine hydrochloride (200 ,ug), yohimbine hydrochloride (22 mg), a combination of the two treatments, and placebo, on some autonomic functions were studied in healthy volunteers using a double-blind crossover design. Clonidine prolonged the recovery time of the light reflex, lowered systolic blood pressure and reduced subjectively rated alertness; these effects were reversed by yohimbine. Responsiveness of sweat glands to carbachol was not affected by the treatments.

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Section: Discussionsupporting

confidence: 92%

“…The attenuation of this effect by yohimbine is consistent with an involvement of central a2-adrenoceptors in clonidine's sedative action (Kooner et al, 1989).…”

Section: Discussionsupporting

confidence: 74%

See 1 more Smart Citation

Effects of clonidine and yohimbine on the pupillary light reflex and carbachol‐evoked sweating in healthy volunteers.

Morley

Bradshaw

Szabadi

1991

Brit J Clinical Pharma

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“…The possibility that the sedative action of clonidine had any effect relevant to the present findings in humans is unlikely. When nitrazepam and clonidine were administered separately to patients in doses that caused similar levels of sedation, nitrazepam evoked no circulatory effect while clonidine did (27).…”

Section: Limitationsmentioning

confidence: 99%

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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“…In humans, circulatory effects of α-2 agonists are independent of any sedative effect: when a benzodiazepine, nitrazepam, induces more sedation than clonidine, no circulatory effect is observed. 18…”

Section: Effects On the Central Nervous System And Ccu Applicationsmentioning

confidence: 99%

Dexmedetomidine and Clonidine

Pichot¹,

Ghignone

Quintin

2011

J Intensive Care Med

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In the critical care setting, α-2 agonists present a multifaceted profile: sedation combined with arousability, suppression of delirium, preservation of respiratory drive, reduced O(2) consumption, preserved renal function, and reduced protein metabolism. In addition, this review details the reduced arterial impedance, improved left ventricular performance, preserved vascular reactivity to exogenous amines, preserved cardiac baroreflex reactivity, preserved vasomotor baroreflex activity combined with a lowered pressure set point: these features may explain the good tolerance observed when α-2 agonists are used as continuous infusion without any loading dose. Reviewing the literature allows one to suggest that a new management appears possible with arousable sedation. However, it remains to be demonstrated whether this arousable sedation can be combined with the preservation of spontaneous ventilation, in the setting of severe respiratory distress, as opposed to conventional controlled mechanical ventilation combined with conventional sedation. Should such a speculative view be confirmed, then α-2 agonists will move from second-line sedative agents to first-line sedative agents. However, key studies are lacking to demonstrate the effect of α-2 agonists on physiological endpoints and outcome. Presently, the existing body of data suggests a niche for the use of α-2 agonists in the critical care setting.

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The haemodynamic and hormonal responses after clonidine occur independently of sedation in essential hypertension.

Cited by 10 publications

References 20 publications

Effects of clonidine and yohimbine on the pupillary light reflex and carbachol‐evoked sweating in healthy volunteers.

Effects of clonidine and yohimbine on the pupillary light reflex and carbachol‐evoked sweating in healthy volunteers.

Effect of clonidine on cardiac baroreflex delay in humans and rats

Dexmedetomidine and Clonidine

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