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

Citation
I. Pohlova et al., 11 beta-hydroxysteroid dehydrogenase activity in spontaneously hypertensive and Dahl rats, AM J HYPERT, 13(8), 2000, pp. 927-933
Citations number
43
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
AMERICAN JOURNAL OF HYPERTENSION
ISSN journal
08957061 → ACNP
Volume
13
Issue
8
Year of publication
2000
Pages
927 - 933
Database
ISI
SICI code
0895-7061(200008)13:8<927:1BDAIS>2.0.ZU;2-W
Abstract
The role of the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) i n hypertension remains unknown even if it appears that the inappropriately decreased 11 beta HSD activity might be involved in a process that leads to high blood pressure. The possible changes of 11 beta HSD were therefore in vestigated 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 co ntaining 0.2% NaCl (DS-LS), and Dahl salt-resistant rats fed the same diets (DR-HS, DR-LS). 11 beta HSD was investigated in colon, aorta, renal cortex , and renal medulla and was assessed as percentage conversion of [H-3]corti costerone to [H-3]11-dehydrocorticosterone in the presence of NAD or NADP. The results demonstrated that genotype exerts a significant effect on 11 be ta HSD. 11 beta HSD activity was significantly increased in colon and renal medulla of SHR compared with WKY rats. No significant differences were obs erved in renal cortex and aorta. In Dahl rats kept on a low-salt diet, 11 b eta HSD activity was significantly higher in colon, renal medulla, and cort ex 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 di et. Increased dietary sodium intake stimulated the activity of 11 beta HSD 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-induce d hypertension is not associated with decreased activity of 11 beta HSD. Ho wever, the results showed that salt intake is able to modulate the activity of 11 beta HSD and that 11 beta HSD in DS and DR rats responds to high die tary salt intake in a different manner. (C) 2000 American Journal of Hypert ension, Ltd.