Background: Salt-sensitive hypertension occurs more commonly in Blacks than in Whites. A decrease in activity of the enzyme 11betaHSD2 that results in overstimulation of the mineralocorticoid receptor by cortisol could contribute to greater retention of sodium in Blacks. We tested the hypothesis that less activity of the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) is present in Blacks than in Whites.
Methods: Eighty-nine subjects (42 Whites and 47 Blacks), ages 12 to 24 years were recruited from a young cohort that was followed longitudinally in a study of blood pressure regulation. For purposes of study, they were admitted to the General Clinical Research Center. Excretion of tetrahydrocortisol (THF), 5alpha-THF, and tetrahydrocortisone (THE) was measured in 12-hour overnight urine collections. In vivo 11betaHSD2 activity was estimated from the urinary (THF + 5alpha-THF)/THE) ratio.
Results: Blacks appeared to retain more sodium as evidenced by a lower level of 2-hour upright plasma aldosterone (P<.001) and marginally lower plasma renin activity (P=.06). The (THF + 5alpha-THF)/THE ratio in Blacks and Whites was similar: 0.91 +/- 0.41 (standard deviation), 0.86 +/- 0.52, 1.13 +/- 0.36, and 0.66 +/- 0.26, in White males, White females, Black males, and Black females, respectively; P=.35 for an overall effect of race. CONDUSION: 11betaHSD2 activity appears to be similar in Blacks and Whites and probably contributes minimally, if at all, to race differences in sodium retention.