Influence of dietary sodium on the renal isoforms of 11 beta-hydroxysteroid dehydrogenase
1997
Brem, A.S. | Bina, R.B. | King Tee. | Chobanian, M.C. | Morris, D.J.
Endogenous glucocorticoids are converted to their biologically inert 11-dehydroderivatives by isoforms of the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD). The low-Km, NAD+-dependent renal isoform (Type 2) identified in the distal nephron protects mineralocorticoid receptors from activation by endogenous glucocorticoids. The function of high-Km, NADP+-dependent renal isoform (Type 1) is less well understood. Since glucocorticoids may modulate sodium transport in renal proximal tubules (PT), we hypothesized that Type 1 activity in this segment may be regulated by dietary Na+. 11 beta-HSD activity was assessed in homogenates of canine PT by the conversion of cortisol to cortisone in the presence of NADP+ 200 micromolar. A high-Na+ diet for 4 days increased the Vmax 4-fold, with no change in the Type 1 Km (40 mEq/day Na+ diet: Km 0.959 micromolar, Vmax 3.40 pmoles/min/mg protein versus 150 mEq/day Na+ diet: Km 0.962 micromolar, Vmax 14.8 pmoles/min/mg protein). Type 1 mRNA also rose in the salt repleted animals. The high-Na+ diet produced no detectable change in the Type 2 isoform enzyme kinetics and mRNA level. No reverse oxo-reductase activity was noted with either renal isoform. Thus, renal Type 1 11 beta-HSD can be regulated by dietary Na+ independent of changes in the renal Type 2 isotorm.
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