11β-hydroxysteroid dehydrogenase activity in spontaneously hypertensive and Dahl rats

The role of the enzyme 11β-hydroxysteroid dehydrogenase (11βHSD) in hypertension remains unknown even if it appears that the inappropriately decreased 11βHSD activity might be involved in a process that leads to high blood pressure. The possible changes of 11βHSD were therefore investigated in rats with spontaneous or salt-induced hypertension. The adult male rats of the following genotypes were used: spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), Dahl salt-sensitive rats fed either a high-salt diet containing 8% NaCl (DS-HS) or low-salt diet containing 0.2% NaCl (DS-LS), and Dahl salt-resistant rats fed the same diets (DR-HS, DR-LS). 11βHSD was investigated in colon, aorta, renal cortex, and renal medulla and was assessed as percentage conversion of [3H]corticosterone to [3H]11-dehydrocorticosterone in the presence of NAD or NADP. The results demonstrated that genotype exerts a significant effect on 11βHSD. 11βHSD activity was significantly increased in colon and renal medulla of SHR compared with WKY rats. No significant differences were observed in renal cortex and aorta. In Dahl rats kept on a low-salt diet, 11βHSD activity was significantly higher in colon, renal medulla, and cortex of DS-LS than in DR-LS rats but no difference was observed in aorta. The differences disappeared in age-matched DS and DR rats fed the high-salt diet. Increased dietary sodium intake stimulated the activity of 11βHSD in renal cortex and medulla of DR rats and decreased the activity in colon of DS rats. We conclude that the development of spontaneous and salt-induced hypertension is not associated with decreased activity of 11βHSD. However, the results showed that salt intake is able to modulate the activity of 11βHSD and that 11βHSD in DS and DR rats responds to high dietary salt intake in a different manner.