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It is primarily used to treat [[increased blood pressure|high blood pressure]], but can also be used for attention deficit hyperactivity disorder, [[anxiety]] disorders, tic disorders, [[drug withdrawal|substance withdrawal]] (from either [[alcohol]], [[opioids]], or smoking tobacco), migraine, [[diarrhea]], and certain pain conditions.<ref>Brayfield, A, ed. (13 January 2014). "Clonidine". Martindale: The Complete Drug Reference. London, UK: Pharmaceutical Press. Retrieved 28 June 2014.</ref>
It is primarily used to treat [[increased blood pressure|high blood pressure]], but can also be used for attention deficit hyperactivity disorder, [[anxiety]] disorders, tic disorders, [[drug withdrawal|substance withdrawal]] (from either [[alcohol]], [[opioids]], or smoking tobacco), migraine, [[diarrhea]], and certain pain conditions.<ref>Brayfield, A, ed. (13 January 2014). "Clonidine". Martindale: The Complete Drug Reference. London, UK: Pharmaceutical Press. Retrieved 28 June 2014.</ref>
Developed for its blood-pressure-lowering effect by Boehringer Ingelheim, clonidine first saw clinical use in 1966. It was the first anti-hypertensive agent with a clearly identifiable central site of action.
Developed for its blood-pressure-lowering effect by Boehringer Ingelheim, clonidine first saw clinical use in 1966.<ref name="Stahle">Stähle, H. (2000). A historical perspective: development of clonidine. Best Practice & Research Clinical Anaesthesiology, 14(2), 237-246. https://doi.org/10.1053/bean.2000.0079</ref> It is the first anti-hypertensive agent with a clearly identifiable central site of action.
Besides its therapeutic value, clonidine has been an important pharmacological tool in research into the role of central α-adrenoceptors in the physiology of central blood pressure regulation.
Besides its therapeutic value, clonidine has been an important pharmacological tool in research into the role of central α-adrenoceptors in the physiology of central blood pressure regulation.<ref name="Stahle" />
Clonidine is classified as a centrally acting α<sub>2</sub> [[adrenergic]] [[agonist]] and imidazoline [[receptor]] [[agonist]]. Its activity on the α<sub>2</sub> receptors in the brainstem inhibits the release of [[norepinephrine]] (NE), resulting in decreased sympathetic tone.<ref>Shen, Howard (2008). Illustrated Pharmacology Memory Cards: PharMnemonics. Minireview. p. 12. ISBN 1-59541-101-1.</ref>
Clonidine is classified as a centrally acting α<sub>2</sub> [[adrenergic]] [[agonist]] and imidazoline [[receptor]] [[agonist]].<ref name="Neil">Neil, MJ (November 2011). "Clonidine: clinical pharmacology and therapeutic use in pain management". Current Clinical Pharmacology. 6 (4): 280–7. https://doi.org/10.2174/157488411798375886. PMID 21827389.</ref><ref name="Stahle" /> Its activity on the α<sub>2</sub> receptors in the brainstem inhibits the release of [[norepinephrine]] (NE), resulting in decreased sympathetic tone.<ref>Shen, Howard (2008). Illustrated Pharmacology Memory Cards: PharMnemonics. Minireview. p. 12. ISBN 1-59541-101-1.</ref>
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.<ref>{{cite journal|last1=van der Kolk|first1=BA|title=The drug treatment of post-traumatic stress disorder.|journal=Journal of Affective Disorders|date=September–October 1987|volume=13|issue=2|pages=203–13|doi=10.1016/0165-0327(87)90024-3|pmid=2960712}}</ref><ref>{{cite journal|last1=Sutherland|first1=SM|last2=Davidson|first2=JR|title=Pharmacotherapy for post-traumatic stress disorder.|journal=The Psychiatric Clinics of North America|date=June 1994|volume=17|issue=2|pages=409–23|pmid=7937367}}</ref><ref>{{cite journal|last1=Southwick|first1=SM|last2=Bremner|first2=JD|last3=Rasmusson|first3=A|last4=Morgan CA|first4=3rd|last5=Arnsten|first5=A|last6=Charney|first6=DS|title=Role of norepinephrine in the pathophysiology and treatment of posttraumatic stress disorder.|journal=Biological Psychiatry|date=November 1999|volume=46|issue=9|pages=1192–204|doi=10.1016/S0006-3223(99)00219-X|pmid=10560025}}</ref><ref>{{cite journal|last1=Strawn|first1=JR|last2=Geracioti|first2=TD, Jr|title=Noradrenergic dysfunction and the psychopharmacology of posttraumatic stress disorder.|journal=Depression and Anxiety|date=2008|volume=25|issue=3|pages=260–71|doi=10.1002/da.20292|pmid=17354267}}</ref><ref>{{cite journal|last1=Boehnlein|first1=JK|last2=Kinzie|first2=JD|title=Pharmacologic reduction of CNS noradrenergic activity in PTSD: the case for clonidine and prazosin.|journal=Journal of Psychiatric Practice|date=March 2007|volume=13|issue=2|pages=72–8|doi=10.1097/01.pra.0000265763.79753.c1|pmid=17414682}}</ref><ref>{{cite journal|last1=Huffman|first1=JC|last2=Stern|first2=TA|title=Neuropsychiatric consequences of cardiovascular medications.|journal=Dialogues in Clinical Neuroscience|date=2007|volume=9|issue=1|pages=29–45|pmid=17506224|pmc=3181843}}</ref><ref>{{cite journal|last1=Najjar|first1=F|last2=Weller|first2=RA|last3=Weisbrot|first3=J|last4=Weller|first4=EB|title=Post-traumatic stress disorder and its treatment in children and adolescents.|journal=Current Psychiatry Reports|date=April 2008|volume=10|issue=2|pages=104–8|doi=10.1007/s11920-008-0019-0|pmid=18474199}}</ref><ref>{{cite journal|last1=Ziegenhorn|first1=AA|last2=Roepke|first2=S|last3=Schommer|first3=NC|last4=Merkl|first4=A|last5=Danker-Hopfe|first5=H|last6=Perschel|first6=FH|last7=Heuser|first7=I|last8=Anghelescu|first8=IG|last9=Lammers|first9=CH|title=Clonidine improves hyperarousal in borderline personality disorder with or without comorbid posttraumatic stress disorder: a randomized, double-blind, placebo-controlled trial|journal=Journal of Clinical Psychopharmacology|date=April 2009|volume=29|issue=2|pages=170–3|doi=10.1097/JCP.0b013e31819a4bae|pmid=19512980}}</ref>
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.<ref>{{cite journal|last1=van der Kolk|first1=BA|title=The drug treatment of post-traumatic stress disorder.|journal=Journal of Affective Disorders|date=September–October 1987|volume=13|issue=2|pages=203–13|doi=10.1016/0165-0327(87)90024-3|pmid=2960712}}</ref><ref>{{cite journal|last1=Sutherland|first1=SM|last2=Davidson|first2=JR|title=Pharmacotherapy for post-traumatic stress disorder.|journal=The Psychiatric Clinics of North America|date=June 1994|volume=17|issue=2|pages=409–23|pmid=7937367}}</ref><ref>{{cite journal|last1=Southwick|first1=SM|last2=Bremner|first2=JD|last3=Rasmusson|first3=A|last4=Morgan CA|first4=3rd|last5=Arnsten|first5=A|last6=Charney|first6=DS|title=Role of norepinephrine in the pathophysiology and treatment of posttraumatic stress disorder.|journal=Biological Psychiatry|date=November 1999|volume=46|issue=9|pages=1192–204|doi=10.1016/S0006-3223(99)00219-X|pmid=10560025}}</ref><ref>{{cite journal|last1=Strawn|first1=JR|last2=Geracioti|first2=TD, Jr|title=Noradrenergic dysfunction and the psychopharmacology of posttraumatic stress disorder.|journal=Depression and Anxiety|date=2008|volume=25|issue=3|pages=260–71|doi=10.1002/da.20292|pmid=17354267}}</ref><ref>{{cite journal|last1=Boehnlein|first1=JK|last2=Kinzie|first2=JD|title=Pharmacologic reduction of CNS noradrenergic activity in PTSD: the case for clonidine and prazosin.|journal=Journal of Psychiatric Practice|date=March 2007|volume=13|issue=2|pages=72–8|doi=10.1097/01.pra.0000265763.79753.c1|pmid=17414682}}</ref><ref>{{cite journal|last1=Huffman|first1=JC|last2=Stern|first2=TA|title=Neuropsychiatric consequences of cardiovascular medications.|journal=Dialogues in Clinical Neuroscience|date=2007|volume=9|issue=1|pages=29–45|pmid=17506224|pmc=3181843}}</ref><ref>{{cite journal|last1=Najjar|first1=F|last2=Weller|first2=RA|last3=Weisbrot|first3=J|last4=Weller|first4=EB|title=Post-traumatic stress disorder and its treatment in children and adolescents.|journal=Current Psychiatry Reports|date=April 2008|volume=10|issue=2|pages=104–8|doi=10.1007/s11920-008-0019-0|pmid=18474199}}</ref><ref>{{cite journal|last1=Ziegenhorn|first1=AA|last2=Roepke|first2=S|last3=Schommer|first3=NC|last4=Merkl|first4=A|last5=Danker-Hopfe|first5=H|last6=Perschel|first6=FH|last7=Heuser|first7=I|last8=Anghelescu|first8=IG|last9=Lammers|first9=CH|title=Clonidine improves hyperarousal in borderline personality disorder with or without comorbid posttraumatic stress disorder: a randomized, double-blind, placebo-controlled trial|journal=Journal of Clinical Psychopharmacology|date=April 2009|volume=29|issue=2|pages=170–3|doi=10.1097/JCP.0b013e31819a4bae|pmid=19512980}}</ref>
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.
Clonidine (known by the trade names Catapres, Kapvay, Nexiclon, Clophelin, and others) is an antihypertensive medication with mild sedative and focus enhancing properties.
It is primarily used to treat high blood pressure, but can also be used for attention deficit hyperactivity disorder, anxiety disorders, tic disorders, substance withdrawal (from either alcohol, opioids, or smoking tobacco), migraine, diarrhea, and certain pain conditions.[1]
Developed for its blood-pressure-lowering effect by Boehringer Ingelheim, clonidine first saw clinical use in 1966.[2] It is the first anti-hypertensive agent with a clearly identifiable central site of action.
Besides its therapeutic value, clonidine has been an important pharmacological tool in research into the role of central α-adrenoceptors in the physiology of central blood pressure regulation.[2]
Clonidine is classified as a centrally acting α2adrenergicagonist and imidazoline receptoragonist.[3][2] Its activity on the α2 receptors in the brainstem inhibits the release of norepinephrine (NE), resulting in decreased sympathetic tone.[4]
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.[5][6][7][8][9][10][11][12]
Binding affinities:
Clonidine shows agonism at the following receptors, namely the alpha (α) receptors. It lowers blood pressure by stimulating the α2 receptors in the brain.[13]
Clonidine also binds to the imidazoline I1 receptor as an agonist.[14]
Some studies suggest that clonidine in low doses can boost growth hormone levels.[15]
Although clonidine overdoses may be reversed by naloxone[citation needed] (a controversial claim) as well as clonidine being noted to cause constipation[16], it causes no respiratory depression.[17]
While the initial hypertensive eect is the expression of peripheral a-adrenoceptor-stimulating properties of the drug, the subsequent and more important decrease in blood pressure is due primarily to a stimulation of central a-adrenoceptors, which causes a reduced activity of the peripheral sympathetic nervous system.
''Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.''
Physical effects
Sedation - Clonidine can be strong in its sedating effect, about equivalent to benzodiazepines. Users can be very tired and can sleep through or ignore prompts to wake up.
Decreased blood pressure - Clonidine's sympatholytic effects lower blood pressure quickly and effectively and therefore, it is commonly used to treat hypertension.[18]
Abnormal heartbeat - Clonidine's chance of causing this is relatively low, but caution should be taken if clonidine is taken with other drugs that can cause this. Intense physical activity should be avoided.
Decreased blood pressure upon standing - This effect may be overwhelming at higher doses and can be described as a "head rush" or feeling of lightheadedness.
Physical fatigue - This general feeling of decreased movement and tiredness is from sedation.
Dizziness - Clonidine can lead to an increased chance of falls due to this. This effect gets stronger with dose increase.
Skin reactions - This can happen if clonidine is given in a patch, such as in Catapres-TTS.
Raynaud's Phenomenon - Raynaud's Phenomenon occurs when the spasm of arteries results in reduced blood flow to the extremities, causing a pale tone, tingling, coldness, and numbness.
Auditory suppression - According to anecdotal reports, this effect is likely due to very low blood pressure, which is why it is listed as physical. It has been described as a "hollow" type distortion or loss of hearing.
Cognitive effects
Cognitive fatigue - Clonidine behaves this way due to the fact that user is usually so sedated that all they want to do is sleep, making cognitive tasks difficult.
Anxiety suppression - Clonidine has relatively strong anxiolytic effects and is sometimes used clinically to treat anxiety.[19]
Focus suppression - This usually occurs at higher doses. The effect is also usually from the sedated state.
Irritability - One can feel very agitated and annoyed, especially with more ease. This especially happens when the medicine is suddenly stopped, which is an incorrect practice; clonidine should be tapered off of the user.
It is strongly recommended that one use harm reduction practices when using this substance. Caution should be used when used in combination with other depressants.
Lethal dosage
According to the NIH prescribing information page for clonidine, clonidine's oral LD50 in mice is 206 mg/kg and for rats, 465 mg/kg.
There are case reports that show naloxone may be a useful antidote in treating clonidine overdoses. However, this is not in widespread clinical use.[20]
Tolerance and addiction potential
Clonidine seems to be able to cause addiction and can be tolerated over periods of time. It is used concurrently with prescription pain-killers (opioids) recreationally because it is reported to have potentiating effects, but this has not been studied and may be dangerous or risky due to oversedation.[citation needed]
Dangerous interactions
Warning:Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
Stimulants (Lisdexamfetamine, amphetamine, propylhexedrine, others) - This combination could potentially increase the chance of an abnormal heartbeat.[citation needed] Caution should be exercised and physical activity should be avoided. However, in clinical use, this combination has a positive effect on the mind, especially in ADHD, and can be used for focusing or memory retention. Still, it is not wise to combine high doses of each substance.[22]
↑Neil, MJ (November 2011). "Clonidine: clinical pharmacology and therapeutic use in pain management". Current Clinical Pharmacology. 6 (4): 280–7. https://doi.org/10.2174/157488411798375886. PMID 21827389.
↑Shen, Howard (2008). Illustrated Pharmacology Memory Cards: PharMnemonics. Minireview. p. 12. ISBN 1-59541-101-1.
↑van der Kolk, BA (September–October 1987). "The drug treatment of post-traumatic stress disorder". Journal of Affective Disorders. 13 (2): 203–13. doi:10.1016/0165-0327(87)90024-3. PMID2960712.
↑Sutherland, SM; Davidson, JR (June 1994). "Pharmacotherapy for post-traumatic stress disorder". The Psychiatric Clinics of North America. 17 (2): 409–23. PMID7937367.
↑Southwick, SM; Bremner, JD; Rasmusson, A; Morgan CA, 3rd; Arnsten, A; Charney, DS (November 1999). "Role of norepinephrine in the pathophysiology and treatment of posttraumatic stress disorder". Biological Psychiatry. 46 (9): 1192–204. doi:10.1016/S0006-3223(99)00219-X. PMID10560025.
↑Strawn, JR; Geracioti, TD, Jr (2008). "Noradrenergic dysfunction and the psychopharmacology of posttraumatic stress disorder". Depression and Anxiety. 25 (3): 260–71. doi:10.1002/da.20292. PMID17354267.
↑Boehnlein, JK; Kinzie, JD (March 2007). "Pharmacologic reduction of CNS noradrenergic activity in PTSD: the case for clonidine and prazosin". Journal of Psychiatric Practice. 13 (2): 72–8. doi:10.1097/01.pra.0000265763.79753.c1. PMID17414682.
↑Najjar, F; Weller, RA; Weisbrot, J; Weller, EB (April 2008). "Post-traumatic stress disorder and its treatment in children and adolescents". Current Psychiatry Reports. 10 (2): 104–8. doi:10.1007/s11920-008-0019-0. PMID18474199.
↑Ziegenhorn, AA; Roepke, S; Schommer, NC; Merkl, A; Danker-Hopfe, H; Perschel, FH; Heuser, I; Anghelescu, IG; Lammers, CH (April 2009). "Clonidine improves hyperarousal in borderline personality disorder with or without comorbid posttraumatic stress disorder: a randomized, double-blind, placebo-controlled trial". Journal of Clinical Psychopharmacology. 29 (2): 170–3. doi:10.1097/JCP.0b013e31819a4bae. PMID19512980.
↑ 13.013.1Isaac, L. (1980). Clonidine in the central nervous system: site and mechanism of hypotensive action. Journal of Cardiovascular Pharmacology, 2, S5-20. PMID: 6154837
↑Bricca, G., Greney, H., Zhang, J., Dontenwill, M., Stutzmann, J., Belcourt, A., & Bousquet, P. (1994). Human brain imidazoline receptors: further characterization with [3 H] clonidine. European Journal of Pharmacology: Molecular Pharmacology, 266(1), 25-33. DOI: https://doi.org/10.1016/0922-4106(94)90205-4
↑Effect of clonidine on growth hormone, prolactin, luteinizing hormone, follicle-stimulating hormone, and thyroid-stimulating hormone in the serum of normal men. (1990). Lal S, Tolis G, Martin SB, Brown GM, Guyda H. https://www.ncbi.nlm.nih.gov/pubmed/1184719
↑Bailey, P. L., Sperry, R. J., Johnson, G. K., Eldredge, S. J., East, K. A., East, T. D., ... & Stanley, T. H. (1991). Respiratory effects of clonidine alone and combined with morphine, in humans. Anesthesiology, 74(1), 43-48.
↑Mitchell A, Bührmann S, Opazo Saez A, Rushentsova U, Schäfers RF, Philipp T, et al. Clonidine lowers blood pressure by reducing vascular resistance and cardiac output in young, healthy males. Cardiovasc Drugs Ther 2005;19:49–55. pmid:15883756
↑Hoehn-Saric R, Merchant AF, Keyser ML, Smith NVK. Effects of Clonidine on Anxiety Disorders. Arch Gen Psychiatry.
↑ Reversal of clonidine toxicity by naloxone. Niemann, James T et al. Annals of Emergency Medicine, Volume 15, Issue 10, 1229 - 1231
↑Koski, A., Ojanperä, I., & Vuori, E. (2002). Alcohol and benzodiazepines in fatal poisonings. Alcoholism: Clinical and Experimental Research, 26(7), 956-959.
What will get this page published? I assume dangerous interactions needs the templates, cite flags, etc. --Corticosteroid (talk) 03:10, 31 August 2017 (CEST)
@corticosteroid: Do you want me to give you instructions or just demonstrate it by completing it myself? Clarity (talk) 22:03, 31 August 2017 (CEST)
. PMID 17506224.