Adrenal steroidogenesis was studied in rats specifically bred for resistance (R) or susceptibility (S), respectively, to the hypertensive effects of salt. S compared to R rats showed higher 18-hydroxydeoxycorticosterone (180HDOC) levels in adrenal venous blood and peripheral plasma. S rat adrenals in vitro produced twice as much 180H-D0C as R rats. The higher 18-hydroxylase activity in S rats was exactly offset by lower llβ-hydroxylation in S rats. This gave rise to characteristic ratios of 18OH-DOC/corticosterone (B) formed in vitro by S and R rat adrenals. Salt feeding did not alter these results. in vitro data from individual rats of several strains suggest that rats fall into 2 phenotypes: those with a high 180H-D0C/B ratio of .65–.80 (S-type) and those with a low ratio of .2–.45 (R-type). Both phenotypes were seen in Sprague-Dawley rats, the strain from which S and R rats were developed. It was concluded that the clear separation of these 2 phenotypes by the selective breeding program which produced the S and R strains was evidence for an effect of 180H-D0C (or the 180H-D0C/B ratio) on blood pressure. Both the spontaneously hypertensive rats of Okamoto and Aoki, and unselected, normotensive Wistar rats had high 180H-D0C/B ratios (S-type). From this fact and other previously published work, it was emphasized in the Discussion that the high 180H-D0C/B ratio of S rats does not in itself explain the total susceptibility of rats to hypertension. In terms of the 180H-D0C/B ratio, it was the low ratio of the resistant rats that appeared to be unique. It was concluded that genetic control of the 180H-D0C/B ratio is probably one of the several genes involved in blood pressure regulation in the rat. (Endocrinology88: 52, 1971)