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      A case report of clonidine induced syncope: a review of central actions of an old cardiovascular drug

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          Abstract

          Background

          Clonidine is an imidazoline sympatholytic, acting on both α 2-adrenergic and imidazoline receptors in the brainstem to induce antihypertensive and negative chronotropic effects in the vasculature and heart respectively.

          Case presentation

          A 69-year-old gentleman with hypertension presented to the emergency department after multiple syncopal episodes over the past 12 months. Electrocardiogram demonstrated sinus bradycardia with a heart rate of 42 beats per minute. It was hypothesized that the antihypertensive agent clonidine was responsible for inducing symptomatic bradycardia. Clonidine was thus gradually tapered and then discontinued over five days restoring normal sinus rhythm rates while avoiding hypertensive rebound related to sympathetic surge. His heart rate and blood pressure remained within normal limits after the clonidine taper and subsequent adjustments to his other hypertensive medications and he was discharged.

          Conclusions

          While clonidine has fallen out of favor for its indication as an antihypertensive, it remains a viable option for the use of opioid withdrawal, chronic pain, and smoking cessation, necessitating the appropriate clinical and pharmacological competencies for a physician to prescribe. A discussion of the clinical effects of clonidine brainstem receptor activation follows.

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          Most cited references 28

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          Alpha(2)-adrenergic receptor signalling in hypertension.

          Cardiovascular regulation by the sympathetic nervous system is mediated by activation of one or more of the nine known subtypes of the adrenergic receptor family; alpha(1A)-, alpha(1B)-, alpha(1D)-, alpha(2A)-, alpha(2B)-, alpha(2C)-, beta(1)-, beta(2)- and beta(3)-ARs (adrenoceptors). The role of the alpha(2)-AR family has long been known to include presynaptic inhibition of neurotransmitter release, diminished sympathetic efferent traffic, vasodilation and vasoconstriction. This complex response is mediated by one of three subtypes which all uniquely affect blood pressure and blood flow. All three subtypes are present in the brain, kidney, heart and vasculature. However, each differentially influences blood pressure and sympathetic transmission. Activation of alpha(2A)-ARs in cardiovascular control centres of the brain lowers blood pressure and decreases plasma noradrenaline (norepinephrine), activation of peripheral alpha(2B)-ARs causes sodium retention and vasoconstriction, whereas activation of peripheral alpha(2C)-ARs causes cold-induced vasoconstriction. In addition, non-selective agonists elicit endothelium-dependent vasodilation and presynaptic inhibition of noradrenaline release. The evidence that each of these receptor subtypes uniquely participates in cardiovascular control is discussed in this review.
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            Advances in Parasympathetic Control of Heart Rate and Cardiac Function.

            It is well known that the neuronal projections from the brain to the heart strongly influence cardiac function, and an abnormal activity has been implicated in diseases such as cardiac arrhythmia and sudden infant death syndrome. This short review describes recent advances focused on the neurobiology of cardiac vagal neurons, utilizing cellular techniques.
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              Role of imidazole receptors in the vasodepressor response to clonidine analogs in the rostral ventrolateral medulla.

              The rostral ventrolateral medulla is the primary site of action for clonidine, a centrally acting antihypertensive. In the rostral ventrolateral medulla, clonidine binds not only to alpha-2 adrenergic receptors but also to specific imidazole sites. In order to determine whether a putative imidazole receptor mediates the hypotensive action of clonidine, a series of compounds was tested 1) in vitro for binding affinity at imidazole and alpha-2 sites and 2) in vivo for ability to lower arterial pressure and heart rate when microinjected directly into the rostral ventrolateral medulla. Hypotensive potency was correlated with affinity at imidazole sites (r = 0.84), but not with alpha-2 affinity (r = -0.05). The bradycardia elicited by this series of compounds also correlated with affinity at imidazole receptors (r = 0.89), but not with alpha-2 affinity (r = 0.10). Furthermore, the imidazole idazoxan selectively reversed the fall in arterial pressure elicited by clonidine, whereas SKF-86466, an alpha-2 antagonist which is not an imidazole, failed to attenuate clonidine's action. An imidazole receptor in the rostral ventrolateral medulla appears to mediate the central hypotensive actions of clonidine and related centrally acting imidazoles and may participate in the regulation of arterial pressure and heart rate.
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                Author and article information

                Contributors
                asand@email.arizona.edu
                m0rris0n@email.arizona.edu
                annespichler@gmail.com
                johnrozich@hotmail.com
                Journal
                BMC Pharmacol Toxicol
                BMC Pharmacol Toxicol
                BMC Pharmacology & Toxicology
                BioMed Central (London )
                2050-6511
                13 February 2018
                13 February 2018
                2018
                : 19
                Affiliations
                [1 ]ISNI 0000 0001 2168 186X, GRID grid.134563.6, University of Arizona, Department of Pharmacology, , College of Medicine, ; 1501 N. Campbell Ave LSN 621, Tucson, AZ 85724 USA
                [2 ]ISNI 0000 0001 2168 186X, GRID grid.134563.6, University of Arizona, Department of Medicine, , College of Medicine, ; Tucson, AZ USA
                [3 ]ISNI 0000 0004 0419 1924, GRID grid.413924.9, Southern Arizona Veterans Affairs Health Care System, ; Tucson, AZ USA
                Article
                198
                10.1186/s40360-018-0198-1
                5810118
                29433586
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                Categories
                Case Report
                Custom metadata
                © The Author(s) 2018

                Toxicology

                basic pharmacology, clonidine, brainstem

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