Central Sympathetic Transmitters and Hypertension

Abstract

1. The aim of this presentation has been to review the current status of some central neurotransmitter mechanisms in the control of arterial blood pressure and in experimental hypertension. In addition, antihypertensive drugs with centrally mediated actions have been considered.2. There is ample evidence for a role of central noradrenaline mechanisms in central cardiovascular regulation. The catecholamine precursor, ~-3,4-dihydroxyphenylalanine, lowers blood pressure by activating sympatho-inhibitory noradrenergic mechanisms in the lower brain stem. The receptors mediating this effect conform to the a-adrenergic type in peripheral tissues. Central noradrenaline receptors also appear to influence blood pressure at suprabulbar levels in the brain. Evidence is accumulating that central adrenergic receptors of the B type are also implicated in cardiovascular control. Central dopamine, 5-hydroxytryptamine and acetylcholine neurons are possibly involved in circulatory regulation but their precise role is less clear at present.3. Considerable work has been done attempting to relate alterations in central neurotransmitter function to arterial hypertension. Central noradrenaline neurons appear to participate in the origin and maintenance of neurogenic hypertension. This may also be the case for other types of experimental hypertension but the results are less conclusive.4. Anti-hypertensive drugs may act by interfering with central neurotransmitter function. The action of ~-a-methyl-3,4-dihydroxyphenylalanine (methyldopa) is largely mediated through an activation by its metabolite, methylnoradrenaline, of noradrenaline mechanisms in the lower brain stem. The central noradrenaline agonist, clonidine, probably acts in an analogous way although some evidence indicates that this drug may influence blood pressure at several levels of central cardiovascular control.

Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata

“…The lower brain stem has been proposed as the primary site of * Present address: National Institute of Public Health, Pharmacology, Laboratory P.O.Box 1, 3720 BA Bilthoven, The Netherlands. action of the blood pressure lowering effect of L-dopa, a-methyldopa and clonidine (for review see Henning, 1973Henning, , 1975Van Zwieten, 1975;. It has been suggested that these drugs act by direct noradrenergic receptor stimulation and may mimic baroreceptor activation (Sinha et al, 1973;Schmitt et al, 1973;Haeusler, 1975;Kobinger and Pichler, 1975).…”

Hyperthyroidism: Specifically increased response to central NA-(?-)receptor stimulation and generally increased monoamine turnover in brain

“…Finally, in view of the strong evidence implicating central NA in cardiovascular control (see Henning, 1975), the apparent sensitization of brain NA-receptors in hyperthyroidism may be related to the concomitant hyperkinetic circulation.…”

Anxiety after Acute Myocardial Infarction and In-Hospital Complications

“…Development of complications is largely responsible for the 10 15% mortality rate in the early stage of AMI (Shah et al, 1994;Swan, 1991). Left ventricular dysfunction (Hendel, 1990), atrial fibrillation (Henning, 1975;Kannel & Abbott, 1987), supraventricular tachycardia (Henning, 1975), left bundle branch block (Henning, 1975), atrioventricular block (Tofler et al, 1987), recurrent ischemia, and reinfarction are common complications associated with in-hospital death.…”