Clonidine: Difference between revisions
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| [[Alpha-1A adrenergic receptor|α<sub>1A</sub>]] || 316.2278 | | [[Alpha-1A adrenergic receptor|α<sub>1A</sub>]] || 316.2278 | ||
Revision as of 16:34, 5 February 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Pratik Bahekar, MBBS [2]
For patient information about Clonidine, click here
Synonyms / Brand Names:
Overview
Not to be confused with clomifene, clonazepam (Klonopin), or clozapine.
Clonidine (trade names Catapres, Kapvay, Nexiclon and others) is a sympatholytic medication used to treat high blood pressure, ADHD, anxiety/panic disorder, and certain pain conditions. It is classified as a centrally acting α2 adrenergic agonist. An alternative hypothesis that has been proposed is that clonidine acts centrally as an imidazoline receptor agonist.
Category
Centrally acting α2 adrenergic agonist.
FDA Package Insert
| Indications and Usage | Dosage and Administration | Dosage Forms and Strengths | Contraindications | Warnings and Precautions | Adverse Reactions | Drug Interactions | Use in Specific Populations | Overdosage | Description | Clinical Pharmacology | Nonclinical Toxicology | Clinical Studies | How Supplied/Storage and Handling | Patient Counseling Information | Labels and Packages
Mechanism of action
Clonidine treats high blood pressure by stimulating α2-receptors in the brain, which decreases peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2-receptors in the vasomotor center in the brainstem. This binding decreases presynaptic calcium levels, thus inhibiting the release of norepinephrine (NE). The net effect is a decrease in sympathetic tone.
It has also been proposed that the antihypertensive effect of clonidine is due to agonism on the I1-receptor (imidazoline receptor), which mediates the sympatho-inhibitory actions of imidazolines to lower blood pressure.
Its mechanism of action in the treatment of ADHD is to increase noradrenergic tone in the prefrontal cortex (PFC) directly by binding to postsynaptic α2A adrenergic receptors and indirectly by increasing norepinephrine input from the locus coeruleus.
| Receptor | Ki (nM) |
|---|---|
| α1A | 316.2278 |
| α1B | 316.2278 |
| α1D | 125.8925 |
| α2A | 42.92 |
| α2B | 106.31 |
| α2C | 233.1 |