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Salt-sensitive subjects (SS) increase their blood pressure with increasing salt intake. Because steroid hormones modulate renal sodium retention, we hypothesize that the activity of the 11␤-hydroxysteroid dehydrogenase type 2 (11␤HSD2) enzyme is impaired in SS subjects as compared with salt-resistant (SR) subjects. The 11␤HSD2 enzyme inactivates 11-hydroxy steroids in the kidney, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids. We performed andoi:10.1210/jcem.84.10.6098 pmid:10523024 fatcat:seltq4ocwbb3nesulh76yfb2dm