抄録
In order to evaluate a role of the sympathetic nervous system in pathogenesis of essential hypertension, urinary excretion of catecholamines was measured and effects of noradrenaline (NA) and sympathetic blocking agents on systemic and digital hemodynamics were observed.
Although daily urinary output of NA, adrenaline (A) and VMA was not increased in most hypertensive patients, diurnal variation of NA and VMA excretion and increase of NA excretion caused by repeated cold pressor tests were higher in the patients than in normotensive subjects.
The maximal rise in pressure induced by intramuscular injection of NA (0.5μg/kg) in the hypertensive group was significantly higher than that in the normotensive group.
Under the basal condition, total peripheral (TPR) and digital vascular resistance (LVR) were significantly greater and digital blood flow (DBF) was significantly lower in the hypertensives.
Intramuscular injection of hexamethonium (C6) gave rise to reduction of blood pressure, TPR and DVR with increase of DBF. These changes were remarkably greater in the hypertensives. NA infusion (0.3μg/kg/min) after pretreatment of C6 resulted in elevation of blood pressure, TPR and DVR with decrease of DBF, while phentolamine injection 0.1 mg/kg resulted in decrease of blood pressure, TPR and DVR with increase of DBF. All of these changes were also significantly greater in the patients with essential hypertension, and there was significant correlation between the response to NA and that to phentolamine.
These results suggested that vascular hyperreactivity to NA might be an etiologic factor in essential hypertension, and that hyper-function of adrenergic α-receptor would play a role, at least in some part, in this vascular reactivity.
