Centrally acting antihypeensive drugs is
Refer kDT 7/e p566 The classic centrally acting antihypeensives such as clonidine, guanfacine and alpha-methyl-DOPA ( its active metabolite alpha-methyl-noradrenaline) induce peripheral sympathoinhibition and a fall in blood pressure as a result of alpha2-adrenoceptor stimulation in the brain stem. These drugs have lost much of their clinical impoance because of their unourable side-effects (sedation, dry mouth, impotence), which are also mediated by alpha2-adrenoceptors, although in other anatomical regions. Moxonidine and rilmenidine are the examples of a new class of centrally acting antihypeensives, which cause peripheral sympathoinhibition mediated by imidazoline (I1)-receptors in the rostral ventromedulla (RVLM). Their side-effect profile appears to be better than that of clonidine and alpha-methyl-DOPA, probably because of a weaker affinity for alpha2-adrenoceptors. The mode of action, haemodynamic profile, antihypeensive efficacy and adverse reactions of the classic and newer centrally acting antihypeensives are the subject of the present survey. Attention is also paid to other therapeutic applications of centrally acting antihypeensives, such as congestive hea failure and the metabolic syndrome.
Phenoxybenzamine
Methyldopa
Prazosin
Propanolol
Cardiovascular system