METUOLI SN OF D , t- ~H-?JOREPINEPHRINE I N ES S ENT I AL HY PERT ENS ION

Defective control of the cardiovascular system by the sympathetic nerves continues to be incriminated as the potential prinary physiologic defect in essential hypertension (EH) . The need to measure synpathetic tone h as progressed from physiologic mensuration by assessment of reflex and pharmacological responses to the recent assay of norepinephrine (NE) and its congeners in both urine and plasma. represents yet another technique by which to evaluate sympathetic function. Previous studies of El1 b this method demonstrated hour tritium accumulation in the urine following I),L-R-3II-NE injection. The present study of 7 normotensive subjects and 7 patients with Eli was designed to depict more precisely t hese abnormalities in 3H-;?E metabolism. FollowinR a one minute injection of 8 pg D,II-B-3H-NE, (200 pCi) intravenouslv, the excretion of unlabeled endogenous metabolites and their labeled congeners was assayed. By these means one could estimate catecholamine svnthesis, turnover of the labeled pools, and by comparison of relative specific activities of the metabolites, gjain some insight into the distribution of the injected material. Alternative catabolic pathways were evaluated by measurement of the excretion of 31120. Patients with EH excreted more label per 24 hours, revealed a more rapid d ecline of 3H2O excretion and lower specific activity of norrnetanephrine (NM). These findings are compatible with changes in pool dynamics and distribution of administered label which gave additional support to the concept of adrenergic dysfunction in association with essential hypertension.