If the patient is on antihypertensive therapy, care should be taken as even a small dose of clonidine may further lower blood pressure and necessitate adjustment of the antihypertensive regimen.
When Clonidine is used as an antihypertensive agent additional clonidine for the prophylaxis of migraine or the alleviation of symptoms in menopausal flushing should not be prescribed. Clonidine may potentiate the effects of alcohol, sedatives, hypnotics or other centrally active substances.
Although retinal, lens or corneal damage have not been detected with clonidine therapy, follow up procedures, such as ophthalmoscopy, are recommended.
Substances which raise blood pressure or induce a sodium and water retaining effect such as nonsteroidal anti-inflammatory drugs can reduce the therapeutic effect of clonidine.
Substances with α2-adrenergic receptor blocking properties, such as phentolamine, may abolish the α2-adrenergic receptor mediated effects of clonidine in a dose-dependent way.
Concomitant administration of drugs with a negative chronotropic or dromotropic effect such as β-blockers or digitalis glycosides can cause or potentiate bradycardic rhythm disturbances.
It cannot be ruled out that concomitant administration of a β-blocker will cause or potentiate peripheral vascular disorders.
The antihypertensive effect of clonidine may be reduced or abolished, and orthostatic regulation disturbances may be provoked or aggravated by concomitant administration of tricyclic antidepressants or neuroleptics with α-receptor blocking effects.
Based on observations in patients in a state of delirium alcoholicum, it has been suggested that high intravenous doses of clonidine may increase the arrhythmogenic potential (QT-prolongation, ventricular fibrillation) of high intravenous doses of haloperidol.
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