1. There is evidence that dysfunction of central adrenergic neurons and the peripheral sympathetic nervous system are implicated in the development and maintenance of spontaneous hypertension.
2. Accordingly adrenoceptors of brain areas related to cardiovascular control (hypothalamus and lower brain stem) and plasma catecholamine levels were measured in male spontaneously hypertensive rats and in their normotensive Wistar-Kyoto controls at 11 weeks of age.
3. Assays of β, α1, and α2 receptor binding were performed by using respectively [3H]-dihydroalprenolol, [3H]clonidine and 3H-labelled WB4101 as ligand. Plasma catecholamines were assessed by high performance liquid chromatography with electrochemical detection.
4. No difference was observed on β-receptor binding sites in the two animal groups. On the other hand, α2 receptors were increased by 29% in the lower brain stem and α1 receptors showed an increase of 46% in the hypothalamus of the hypertensive rats. By Scatchard plot analysis, these changes were attributable to variations in the number rather than in the affinity of binding site.
5. Plasma noradrenaline levels were more elevated in the hypertensive rats, and no difference was observed in plasma adrenaline concentrations.
6. The increase in hypothalamic α1 receptors and the probably compensatory increase in lower brain stem α2 receptors suggest enhanced stimulation of the vasomotor centre. Hyperactivity of the peripheral sympathetic nervous system in spontaneous hypertension could therefore be secondary to a dysfunction of central adrenergic neurons projecting to the vasomotor centre of the brain stem.
