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- W52064124 abstract "Classic centrally acting antihypertensive drugs such as clonidine, guanfacine and alpha-methyl-dioxyphenylalanine (alpha-methyl-DOPA) (via its active metabolite alpha-methyl-noradrenaline) are assumed to induce peripheral sympathoinhibition and a reduction in (elevated) blood pressure as a result of the stimulation of alpha2-adrenoceptors in the pons-medulla region in the brain. Their antihypertensive efficacy is beyond doubt, but their profile of adverse reactions is considered unfavourable when compared with most other antihypertensive drugs currently used, such as low-dose diuretics, beta-blockers, angiotensin-converting enzymes (ACE)-inhibitors, calcium antagonists, peripheral alpha1-adrenoceptor antagonists, and angiotensin II-receptor antagonists. More recently, central imidazoline (I1)-receptors have been recognized to be another target of centrally acting antihypertensive drugs. Clonidine is considered at present to be a mixed agonist that stimulates both alpha2- and I1-receptors. Moxonidine and rilmenidine are considered to be moderately selective I1-receptor stimulants, although it still remains unknown whether these agents act directly on the receptor as genuine agonists. The imidazoline (I1)-agonists also cause peripheral sympathoinhibition, triggered at the level of central nervous imidazoline receptors, predominantly in the rostral ventrolateral medulla. The imidazoline receptor stimulants are effective antihypertensives with a mode of action and haemodynamic profile which seems attractive from a pathophysiological point of view. Moxonidine and rilmenidine are considered preferable over the classic alpha2-adrenoceptor stimulants because of their pattern of side-effects, which may be explained on the basis of absent or weak affinity for the alpha2-adrenoceptor." @default.
- W52064124 created "2016-06-24" @default.
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- W52064124 date "1999-08-01" @default.
- W52064124 modified "2023-09-23" @default.
- W52064124 title "The renaissance of centrally acting antihypertensive drugs." @default.
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