1. A survey is given of the various aspects of centrally acting hypotensive drugs. The majority of centrally acting hypotensive agents act by way of central alpha-adrenoceptors, probably located in the pontomedullary region of the brain. These central receptors are stimulated by clonidine, guanfacine and various related compounds, and also by alpha-methylnoradrenaline, generated in vivo upon biotransformation of alpha-methyldopa within the brain. The stimulation of the alpha-adrenoceptors induces a decrease in peripheral sympathetic tone and thus a fall in arterial blood pressure and bradycardia. 2. The possibility that presynaptic alpha-adrenoceptors in the brain are involved in the central hypotensive action of clonidine, guanfacine and related compounds is discussed. Also, the possible involvement of central histaminergic and cholinergic receptors in central hypotensive effects is reviewed. 3. Various experimental compounds with a central hypotensive effect different from that of clonidine and related drugs are mentioned. 4. Finally, it is pointed out that the hypotensive effects of various beta-sympatholytic drugs and of prazosin are probably not of central origin.