Central nervous system

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Clonidine (Catapres) is an imidazoline which is an agonist to a2-adrenoceptors (postsynaptic) in the brain, stimulation of which suppresses sympathetic outflow and reduces blood pressure. At high doses it also activates peripheral a2-adrenoceptors (presynaptic autoreceptors) on the adrenergic nerve ending; these mediate negative feedback suppression of noradrenaline release. In overdose clonidine can stimulate peripheral a^-adrenoceptors (postsynaptic) and thus cause hypertension by vasoconstriction. Clonidine was discovered to be hypotensive, not by the pharmacologists who tested it in the laboratory but by a physician who used it on himself as nose drops for a common cold.24 The is 6 h.

Clonidine reduces blood pressure with little postural or exercise related drop. Its most serious handicap is that abrupt or even gradual withdrawal causes rebound hypertension. This is characterised by plasma catecholamine concentrations as high as those seen in hypertensive attacks of phaeochro-mocytoma. The onset may be rapid (a few hours) or delayed for as long as 2 days; it subsides over 2-3 days. The treatment is either to reinstitute clonidine, i.m. if necessary, or to treat as for a phaeochro-mocytoma. Clonidine should never be used with a p-adrenoceptor blocker which exacerbates withdrawal hypertension (see phaeochromocytoma). Common

23 Page L H 1981 New England Journal of Medicine 304:1371. The eminent pharmacologist, Sir John Gaddum, also dubbed the characteristic appearance as 'hexamethonium man'.

24 Page L H 1981 New England Journal of Medicine 304:1371.

adverse effects include sedation and dry mouth. Tricyclic antidepressants antagonise the antihypertensive action and increase the rebound hypertension of abrupt withdrawal. Low dose clonidine (Dixarit, 50-100 microgram/d) also has a minor role in migraine prophylaxis, menopausal flushing and choreas.

Rebound hypertension is a less important problem with longer-acting imidazolines, since omission of a single dose will not trigger the rebound. Such drugs include moxonidine and rilmenidine. These drugs are said to be selective for an imidazoline receptor, rather than a2-receptor. However, no such receptor has been identified at the molecular level, and genetic knockout experiments have shown that it is the a2-receptor which is required for the blood pressure lowering action of imidazoline drugs. It is unsurprising therefore that no drug has truly succeeded in separating the sedative and hypotensive effects of this class.

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