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Clonidine is a medication that is used to treat high blood pressure, attention deficit hyperactivity disorder, anxiety disorders, tic disorders, withdrawal (from either alcohol, opioids, or smoking ), migraine, menopausal flushing, diarrhea, and certain pain conditions. It is marketed under many brand names.
The adverse effects include sedation, dry mouth, and low blood pressure.
Clonidine treats high blood pressure by stimulating α 2 receptors in the brain stem, which decreases peripheral vascular resistance, lowering blood pressure. Clonidine also may cause bradycardia, probably by increasing signaling through the vagus nerve. When given intravenously, clonidine temporarily increases blood pressure by stimulating postsynaptic α 2 receptors in smooth muscle in the lining of blood vessels. This does not occur when clonidine is given by mouth or transdermally. : 201–203
It has been in use as a medication since 1966.
1 Medical uses
1.1 Clonidine suppression test
2 Adverse effects
3.1 Mechanism of action
3.1.1 High blood pressure
3.1.2 Attention deficit hyperactivity disorder
3.1.3 Growth hormone test
4 Brand names
6 External links
Clonidine tablets and transdermal patch
Clonidine was introduced in 1966.
Clonidine may be used to ease withdrawal symptoms associated with the long-term use of narcotics, alcohol, benzodiazepines and nicotine (smoking).
Clonidine also has several off-label uses, and has been prescribed to treat psychiatric disorders including stress, sleep disorders, and hyperarousal caused by post-traumatic stress disorder, borderline personality disorder, and other anxiety disorders.
Clonidine suppression test
The reduction in circulating norepinephrine by clonidine was used in the past as an investigatory test for phaeochromocytoma, which is a catecholamine-synthesizing tumour, usually found in the adrenal medulla.
Clonidine is classed by the FDA as pregnancy category C. It is classified by the TGA of Australia as pregnancy category B3, which means that it has shown some detrimental effects on fetal development in animal studies, although the relevance of this to human beings is unknown.
The principal adverse effects of clonidine are sedation, dry mouth, and hypotension (low blood pressure).
Adverse effects by frequency
Very common (>10% frequency):
Xerostomia (dry mouth)
Skin reactions (if given transdermally)
Common (1-10% frequency):
Pain below the ear (from salivary gland)
Uncommon (0.1-1% frequency):
Rare (<0.1% frequency): Gynaecomastia Impaired ability to cry Atrioventricular block Nasal dryness Colonic pseudo-obstruction Alopecia Hyperglycaemia Withdrawal Clonidine suppresses sympathetic outflow resulting in lower blood pressure, but sudden discontinuation can cause rebound hypertension due to a rebound in sympathetic outflow. Clonidine therapy should generally be gradually tapered when discontinuing therapy to avoid rebound effects from occurring. Treatment of clonidine withdrawal hypertension depends on the severity of the condition. Reintroduction of clonidine for mild cases, alpha and beta blockers for more urgent situations. Beta blockers never should be used alone to treat clonidine withdrawal as alpha vasoconstriction would still continue. Pharmacology Mechanism of action Receptor K i (nM) Alpha-1A adrenergic receptor 316.23 Alpha-1B adrenergic receptor 316.23 Alpha-1D adrenergic receptor 125.89 Alpha-2A adrenergic receptor 42.92 Alpha-2B adrenergic receptor 106.31 Alpha-2C adrenergic receptor 233.1 The K i refers to a drug's affinity for a receptor. The smaller the K i, the higher the affinity for that receptor. High blood pressure Clonidine treats high blood pressure by stimulating α 2 receptors in the brain stem, which decreases peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α 2 receptors in the vasomotor center in the brainstem. This binding has a sympatholytic effect, suppresses release of norepinephrine, ATP, renin, and neuropeptide Y which if released would increase vascular resistance. : 201–203 Clonidine also acts as an agonist at imidazoline-1 (I 1 ) receptors in the brain, and it is hypothesized that this effect may contribute to reducing blood pressure by reducing signaling in the sympathetic nervous system, but this effect acts upstream of the central α 2 agonist effect of clonidine. Clonidine also may cause bradycardia, probably by increasing signaling through the vagus nerve. When given intravenously, clonidine can temporarily increase blood pressure by stimulating α 1 receptors in smooth muscles in blood vessels. : 201–203 Attention deficit hyperactivity disorder Structural comparison between the neurotransmitter norepinephrine and the drug clonidine. Both drugs bind to alpha-2 adrenergic receptors. Similarities between the two structures are shown highlighted in red. In the setting of attention deficit hyperactivity disorder (ADHD), clonidine's molecular mechanism of action occurs due to its agonism at the alpha-2A adrenergic receptor, the subtype of the alpha-2 adrenergic receptor that is most principally found in the brain. Within the brain, the alpha-2A adrenergic receptors are found within the prefrontal cortex (PFC), among other areas. The alpha-2A adrenergic receptors are found on the presynaptic cleft of a given neuron, and, when activated by an agonist, the effect on downstream neurons is inhibitory. The inhibition is accomplished by preventing the secretion of the neurotransmitter norepinephrine. Thus, clonidine's agonism on alpha-2A adrenergic receptors in the PFC inhibits the action of downstream neurons by preventing the secretion of norepinephrine. This mechanism is similar to the brain's physiological inhibition of PFC neurons by the locus ceruleus (LC), which secretes norepinephrine into the PFC. Although norepinephrine can also bind to target adrenergic receptors on the downstream neuron (otherwise inducing a stimulatory effect), norepinephrine also binds to alpha-2A adreneric receptors (akin to clonidine's mechanism of action), inhibiting the release of norepinephrine by that neuron and inducing an inhibitory effect. Because the PFC is required for working memory and attention, it is thought that clonidine's inhibition of PFC neurons helps to eliminate irrelevant attention (and subsequent behaviors), improving the person's focus and correcting deficits in attention. Growth hormone test Clonidine stimulates release of growth hormone releasing hormone from the hypothalamus, which in turn stimulates pituitary release of growth hormone. Pharmacokinetics After being ingested, clonidine is absorbed into the blood stream rapidly and nearly completely, with peak concentrations in human plasma occurring within 60–90 minutes. Brand names As of June 2017 clonidine was marketed under many brand names worldwide: Arkamin, Aruclonin, Atensina, Catapin, Catapres, Catapresan, Catapressan, Chianda, Chlofazoline, Chlophazolin, Clonid-Ophtal, Clonidin, Clonidina, Clonidinã, Clonidine, Clonidine hydrochloride, Clonidinhydrochlorid, Clonidini, Clonidinum, Clonigen, Clonistada, Clonnirit, Clophelinum, Dixarit, Duraclon, Edolglau, Haemiton, Hypodine, Hypolax, Iporel, Isoglaucon, Jenloga, Kapvay, Klofelino, Kochaniin, Melzin, Menograine, Normopresan, Paracefan, Pinsanidine, Run Rui, and Winpress.
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