Much of our knowledge about the CNS control of blood pressure is derived from animal studies using techniques such as intracerebroventricular administration of drugs, stereotactic ablation of specific brain nuclei, and biochemical analysis of these nuclei. These methods have identified numerous specific brain nuclei in the brain stem and a meshwork of interconnecting neurones involved in cardiovascular control. The main neurotransmitter involved is noradrenaline but recent interest has focused on several laterally situated nuclei which are capable of synthesizing adrenaline. Centrally acting antihypertensive drugs are thought to act by stimulating central alpha 2-adrenoceptors either by the parent drug itself (clonidine) or via the formation of an active metabolite (alpha-methyldopa). This leads to decreased peripheral sympathetic activity and a hypotensive response but the latter is often attained at the expense of central side-effects such as drowsiness or dry mouth. The mechanism of the antihypertensive effect of beta-blockers remains uncertain although the balance of evidence is against a central effect. The central administration of propranolol causes decreased peripheral sympathetic activity in animals, but plasma catecholamine levels are little altered by beta-blockers in man. In equipotent antihypertensive doses, central alpha-agonists cause a much greater reduction in plasma noradrenaline than beta-blockers.
Struthers, A. D., & Dollery, C. T. (1985). Central nervous system mechanisms in blood pressure control. European Journal of Clinical Pharmacology, 28(1 Suppl.), 3-11. https://doi.org/10.1007/BF00543703