We previously showed that adrenal renin is highest in the rat zona glomerulosa (ZG) and that low sodium or high potassium and nephrectomy increase adrenal ZG renin and aldosterone. Dahl salt-sensitive rats (S) have been shown to have lower plasma renin activity and plasma aldosterone and higher plasma 18-hydroxy-ll-deoxycorticosterone than Dahl salt-resistant rats (R). In this study we assess the possible role of adrenal ZG renin in the suppression of aldosterone in S rats. Adrenal ZG renin was significantly decreased in S as compared with R rats even at 6 weeks of age, when both S and R rats are still normotensive (S = 7.2 ± 0.2, R = 18.0 ± 1.6 ng angiotensin I/mg protein/hr). Adrenal ZG aldosterone was also significantly lower in S than in R rats (S = 21.1 ± 4.3, R = 39.5 ± 3.6 ng/mg protein). Furthermore, the rise in adrenal ZG renin and aldosterone after nephrectomy in S rats was significantly less than that in R rats. To determine if the suppressed adrenal ZG renin of S rats is due to volume expansion, we studied the effect of a sodium-deficient diet on adrenal ZG renin in S and R rats. After 2 weeks of a sodium-deficient diet S rats had significantly lower basal adrenal ZG renin than did R rats (S = 7.6 ± 0.4, R = 21.7 ± 1.9 ng angiotensin I/mg protein/hr) and a marked blunting of the adrenal ZG renin response to nephrectomy (S = 13.6 ± 1.1, DR = 167 ± 16.1 ng angiotensin I/mg protein/hr). Our previous report of blunting of the nephrectomy response by indomethacin suggests a role for prostaglandins in the regulation of adrenal renin. Adrenal ZG prostaglandin E2in S rats was also significantly lower than in R rats (S = 0.22 ± 4.3, R = 0.40 ± 0.05 ng/mg protein). These data indicate that the low adrenal ZG renin in S rats is associated with low plasma aldosterone and that the low adrenal ZG renin level of S rats is not due to volume expansion and probably represents a genetic abnormality of the salt-sensitive strain or the low adrenal ZG prostaglandin E2level, or both.