To assess the role of the sympathetic and central noradrenergic neurons in one-and two-kidney Goldblatt hypertension, we examined the concentration and turnover of norepinephrine (NE) in the aorta, mesenteric artery, left ventricle, hypothalamus, midbrain, and pons medulla of hypertensive and control rabbits. Animals were made hypertensive by constriction of the left renal artery after right nephrectomy (1KGH group) or with the right kidney left intact (2KGH group), or were sham-operated on the renal artery (1KGC and 2KGC groups). At 14 days after the constriction, the blood pressure was increased to 136 ± 3 mm Hg in the 1KGH vs 98 ± 3 mm Hg in the 1KGC (p < 0.001), and 136 ± 2 mm Hg in the 2KGH vs 94 ± 2 mm Hg in the 2KGC group [p < 0.001). Turnover time in the aorta, mesenteric artery, and left ventricle in the 1KGH group was decreased to 47%, 45%, and 65% of that in the 1KGC group, respectively. Results suggest that enhanced sympathetic neuron activity in the cardiovascular system, especially in the arteries, contributes to the development of one-kidney Goldblatt hypertension. Norepinephrine turnover in the cardiovascular tissues in the 2KGH group and in the brain stem in the 1KGH and 2KGH group was not different from that in the control group. (Hypertension 4: 272-278, 1982) KEY WORDS • norepinephrine turnover • cardiovascular tissues * brain stem one-kidney Goldblatt hypertension • two-kidney Goldblatt hypertension T WO types of renovascular hypertension in the rabbit, one-kidney Goldblatt (1KG) and two-kidney Goldblatt (2KG), show several contrasting features in pathophysiology, e.g., in serum potassium level, plasma renin activity, hematocnt, and circulating blood volume, 1 " 8 or in the incidence of cerebral hemorrhage. 4 It has been postulated that underlying pathogenetic mechanisms are also different between these two models of hypertension." Hyperactivity of the sympathetic neurons has been implicated as one of the causal factors in experimental as well as essential hypertension. chronic 1 KG hypertensive dogs, norepinephrine (NE) turnover was decreased in the kidney and normal in the heart,* and in chronic 2KG hypertensive rats, was slightly increased in the heart. 10 Recently, Reid et al. 11 reported that plasma NE levels are high in acute 1K.G hypertension in the rat but normal in 2KG hyperten-sion, indicating variable contribution of the sympathetic neurons. No data on NE turnover are available for the acute stage of Goldblatt hypertension, however. There is a body of evidence that central noradren-ergic mechanisms are also involved in hyperten-sion. 11 " 14 Norepinephrine turnover in the central nervous system decreased in deoxycorticosterone (DOC)-sodium hypertension 15 " 18 and increased in sino-aortic denervation hypertension, 17 and the altered activity of the central noradrenergic neurons has been considered a primary abnormality initiating hyper-tension. Again, there is a paucity of information about Goldblatt hypertension. In the present study, we examined NE turnover in the cardiovascular...