SUMMARY Attempted correction of two-kidney, one clip Goldblatt hypertension in the rat was carried out by three techniques: removal of the constricting dip, removal of the Iscberaic kidney, and converting enzyme blockade by oral captopril. Since duration of hypertension is said to be a critical factor, groups of rats were studied after short term (< 6 weeks from clipping) and chronic (> 4 months) hypertension. Blood pressure, sodium balance, and plasma renin concentration (PRC) were followed before and after these correcting procedures. In a control group of animals, removal of a loose renal artery clip did not Influence blood pressure and only caused trivial postoperative retention of sodium. Undipptng, however, normalized blood pressure in both short-term and chronic hypertension. After a major postoperative fall, blood pressure returned to somewhat elevated levels after nephrectomy in animals with chronic (but not short-term) hypertension. Sodium balance became markedly positive with the fall in blood pressure of operated hypertensive anlmpu and was significantly correlated with the fall in blood pressure in these four groups at 7 days (r= 0.43). Captopril also produced a fall in blood pressure at 24 hours, with a positive sodium balance, although the relationship between blood pressure fall and sodium balance did not reach statistical significance (r= 0 JO). The PRC was elevated in all hypertensive groups, although individual values overlapped with values from normal rats and nonhypertensive rats with a loose renal artery dip. The PRC fell to normal or subnormal values after either operative procedure and stabilized for at least 2 months Independently of whether blood pressure fell or not. It is concluded that neither sodium retention nor renin hypersecretion maintains blood pressure In this model. Also, the rapidity of the blood pressure fall is not consistent with a role for vascular hypertrophy. Tbe greater efficacy of unclipping suggests that the revascularized kidney after this procedure exerts a vasodepressor function independent of sodium excretion or the renin-angiotensin system.