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.