Prerious evidence shows that salthyphensensitive (S) rats have a net increase in plasma mlneralocorticoid activity due to l & -hydroxyhyphenll-deoxycorticosterone and decreased urinary kallikrein excretion compared to salthyphenresistant (R) rats. Since minermlocorticolds stimulate urinary kallikrein excretion, these results are inconsistent. This inconsistency was explained by the fact that, while R rats responded normally to treatment with deoxycorticosterone (DOC) by an Increase in urinary kallikrein excretion, S rats showed no change in urinary kallikrein even when treated with 10 mg of DOC/day for 24 days. S and R rats responded identically to DOC with changes in muscle electrolytes and relative hypertrophy of the renal distal tubule. Other measures of chronic mlneralocorticoid response in S rats beside kallikrein were, therefore, intact. It was found that S rats were capable of responding to Na deficient diet with an increase in urinary kallikrein comparable to R rats. It was argued, therefore, that mineralcocorticoid receptor mechanisms and distalhyphentubular cell responsiveness are intact in S rats. Mild glomerular and tubular scarring was found in S rats and the severity of renal lesions was increased by DOC treatment in S rats. These lesions correlated well with blood pressure and protelnuria. No such lesions were present in control or DOC treated R rats. It was suggested that failure of urinary kallikrein to respond to DOC in S rats may be a secondary phenomenon resulting from renal damage. (Hypertension 4: 20–26, 1982)