Central catecholaminergic nerves have an integral place in the central connections of the autonomic nervous system, and they play an important role in the regulation of arterial blood pressure. Some evidence suggests that central serotonergic nerves also participate in the control of blood pressure. Studies in various models of experimental hypertension have demonstrated changes in the metabolism and the activity of these central monoaminergic nerves. In addition, selective ablation of central catecholaminergic or serotonergic nerves with a variety of chemical compounds profoundly modifies the development of high blood pressure in a number of experimental models. It seems clear that central monoaminergic systems participate in the regulation of normal blood pressure and that their function is altered in experimental hypertension. However, the exact significance of these changes in experimental hypertension has not been established. Moreover, it is not yet clear which changes are of primary causal importance and which are secondary in nature. There are definite qualitative and quantitative differences in the activity of central monoaminergic nerves in these models of experimental hypertension and in normal animals. These differences are manifest in the markedly different patterns of central monoamine metabolism and the different central effects of selective antagonists on arterial blood pressure in the various preparations. It is clearly not tenable to regard all of these central circulatory effects as nonspecific sequelae of interference with central aminergic tracts participating normally in the normal control of arterial blood pressure. Central catecholaminergic nerves play an important role in the regulation of arterial blood pressure. Although they appear to have little importance in the maintenance of resting arterial blood pressure in normal unstressed animals, they play a major role in the reflex control of blood pressure through the arterial baroreceptor reflexes. The activity of bulbospinal noradrenergic nerves appears to facilitate the increase in arterial blood pressure in neurogenic hypertension and possibly in deoxycorticosterone (DOCA) salt hypertension. The activity of brain stem catecholaminergic nerves appears to inhibit the activity of bulbospinal noradrenergic and serotonergic nerves and hence to have a depressor effect on arterial blood pressure. Disinhibition of bulbospinal noradrenergic and serotonergic fibers by deafferentation of arterial baroreceptors (neurogenic hypertension) or by decreased activity of inhibitory catecholaminergic nerves in the brain stem (DOCA salt and renal hypertension) could play a significant role in the pathogenesis of experimental hypertension. The participation of central catecholaminergic nerves in genetic hypertension (the spontaneously hypertensive rat) has not yet been established. Central serotonergic nerves also appear to play a significant role in the regulation of arterial blood pressure in normal animals and in some models of experimental hypertension. The activity of bulbo spinal serotonergic nerves seems to facilitate the maintenance of arterial blood pressure in normal animals and the increase in blood pressure in experimental neurogenic hypertension, although this matter is still controversial. Central serotonergic nerves do not appear to contribute to experimental renal hypertension, but they may play a role in elevating the pressure in the spontaneously hypertensive rat. The central connections of the autonomic nervous system utilize a variety of neurotransmitters in much the same way as do the peripheral components. It should be expected that each of these central neurotransmitters can be facilitatory or inhibitory in different pathways and that each can synapse with a variety of functionally distinct receptors. These facts, with the presence of short excitatory or inhibitory interneurons, increase the complexity of experimental data on the functional role of central monoaminergic pathways.