Catecholamines, sodium and renin in unilateral renal hypertension in man.

The relative roles of plasma or urinary norepinephrine (NE) and epinephrine (E), exchangeable sodium, blood volume, and plasma renin (PRA) or aldosterone in the pathogenesis of unilateral renal hypertension was evaluated. 99 normal subjects and 33 age-matched untreated hypertensive patients with unilateral renal parenchymal disease (RPD) (n = 18) or unilateral renal artery stenosis (RAS) (n = 15) were compared. Measurements were repeated following operative treatment in 23 patients. Plasma and urinary NE or E, exchangeable sodium and blood volume did not differ significantly between normal and untreated subjects with RPD or RAS. Both patient subgroups had increased blood pressure and supine PRA (p less than 0.001); these abnormalities were milder with RPD. Plasma aldosterone and upright PRA were significantly elevated (p less than 0.05) in RAS only. Operative treatment of RPD and RAS caused decreases in blood pressure (-18 and -28%) and PRA; they correlated in RPD (r = 0.56; p less than 0.05). In RPD and RAS, exchangeable sodium, blood volume, and NE or E values were not significantly changed following operation, except for mildly increased upright PNE in RAS. These observations suggest that the sympathetic system plays no major role in the maintenance of unilateral renal hypertension in man. However, the 'normal' body sodium-volume state in RPD or RAS may be inappropriate relative to coexisting hypertension. In addition to its established role in RAS, mild activation of the renin-angiotensin system may also be important for the pathogenesis of hypertension caused by unilateral RPD.