Clonidine

Clonidine is a central alpha-2 receptor agonist and belongs to the drug group of antisympathotonics. Clonidine was originally developed to treat arterial hypertension and is now also used to treat attention deficit/hyperactivity disorder ADHD.

In ophthalmology it is used as eye drops to treat increased intraocular pressure.

The group of alpha2-adrenoreceptor agonists also includes:

• Moxonidine
• and
• alpha-methyldopa.

The imidazolidine derivative clonidine acts as a central alpha-2 receptor agonist, resulting in a reduction of sympathetic nervous system activity and an increase in vagotonic tone. Both effects lead first to a reduction in cardiac output by lowering the heart rate and then to a reduction in peripheral resistance. Blocking peripheral presynaptic alpha-2 receptors also leads to a reduction in norepinephrine secretion.

In the eye, clonidine reduces intraocular pressure when applied locally. This is achieved by improving the outflow of aqueous humor through contraction of the muscle fibers of the ciliary muscle. This opens the Schlemm's canal. The aqueous humor can flow off better. In addition, clonidine eye drops lead to a slight reduction in the production of aqueous humor.

Clonidine is well absorbed orally with an oral bioavailability of 75 to 100 percent. Clonidine is rapidly distributed in the tissue, passes the blood-brain barrier due to its high lipophilicity. The elimination half-life is subject to considerable inter-individual fluctuations; it is 8 to 15 hours and can be up to 30 hours depending on kidney function. Within 96 hours, about 70 percent of the orally administered clonidine is eliminated renally, of which 60 % of the dose is unmetabolized. A small portion is metabolized in the liver. The main metabolite p-hydroxy clonidine is pharmacologically inactive and accounts for 7 to 10% of the eliminated amount. 20% of the total amount is excreted in the faeces.

Clonidine is available in tablet form, as retardation capsules, as eye drops and as an injection solution.

When administered orally, clonidine is used to treat arterial hypertension, provided that it is not caused by a pheochromocytoma. In the form of eye drops, clonidine is used to treat ocular hypertension and all forms of glaucoma. Here, a reduction in intraocular pressure occurs 15 to 30 minutes after clonidine eye drops are administered, is fully developed after about 2 hours and lasts 8 to 12 hours.

Clonidine is used as an injection to treat the symptoms of sympathoadrenergic hyperactivity (tremor, tachycardia, hypertension, sweating, agitation, tachypnea) in the context of acute alcohol withdrawal syndrome.

Clonidine must not be used during pregnancy and lactation. Clonidine passes through the placenta. In the fetus there may be a reduction in the heart rate. In individual cases a temporary increase in blood pressure has been observed in the newborn post partum. There is insufficient experience regarding the long-term effects of prenatal exposure.

Clonidine should not be used during lactation because clonidine passes into breast milk and there are insufficient data on use during lactation.

Dosage: 150μg

Very often (≥ 1/10) it occurs under the application of clonidine:

• Vertigo
• Sedation
• Orthostatic hypotension
• Dry mouth

Common (≥ 1/100 to < 1/10) are the side effects:

• Depression
• Insomnia
• Headaches
• constipation, nausea, vomiting, pain in the salivary glands
• erectile dysfunction
• Tiredness

The following interactions exist for clonidine:

• Neuroleptics of the phenothiazine or butyrophenone type cardiotoxic effect of the neuroleptic (e.g. prolongation of the QT time, ventricular fibrillation) can be enhanced and lead to threatening ventricular arrhythmias, especially in pre-damaged myocardium.
• Neuroleptic drugs of the phenothiazine or butyrophenone type Cardiotoxic effect of the neuroleptic (e.g. prolongation of the QT time, ventricular fibrillation) can be intensified and lead to threatening ventricular arrhythmias, especially in the case of pre-damaged myocardium.
• Antihypertensive drugs, vasodilatants or diuretics Enhancement of the blood pressure-lowering effect is possible.
• Beta-blockers Bradycardias and cardiac arrhythmias (AV block) possible. It cannot be ruled out that peripheral vascular disease is triggered or intensified.
• Cardiac glycoside bradycardias and AV dissociations possible.
• Tricyclic antidepressants, blood pressure increasing or sodium and water retaining substances, e.g. non-steroidal antirheumatic drugs A weakening of the blood pressure lowering effect is possible
• Centrally attenuating drugs (hypnotics, sedatives); effect is mutually amplified or unpredictably altered.
• Alpha-2-receptor blockers such as tolazoline or phentolamine Antihypertensive effect of clonidine hydrochloride is weakened or cancelled by tolazoline or phentolamine.
• pharmacologically similar acting substances such as α-methyldopa, guanfacine, guanabenz or reserpine

Hypersensitivity to the active substance

Certain excitation formation and conduction disorders of the heart, e.g. sinus node syndrome or AV block II and III

Heart rate < 50 / minute (bradycardia)

Major Depression (depressive disorder)

Pronounced hypotension; hypovolemia-induced hypotension must be compensated before therapy begins

Catapresan®, 150 micrograms/ml, solution for injection