The present study was aimed at investigating the role of type II 11β-hydroxysteroid
dehydrogenase (IIβ-HSD II) in the development of
hypertension. Two-kidney, one-
clip (2K1C),
deoxycorticosterone acetate (
DOCA)/
salt, or
N (G)-nitro-L-arginine methyl ester (
L-NAME)
hypertension was induced in male Sprague-Dawley rats. Four weeks later, the expression of 11β-HSD II
mRNA was determined in the kidney by Northern blot analysis. The plasma level of
aldosterone was measured by radioimmunoassay. In 2K1C
hypertension, the expression of 11β-HSD II was decreased in the clipped kidney and increased in the non-clipped kidney. The expression was increased in the remnant kidney of
DOCA/
salt hypertension, while decreased in the kidneys of
L-NAME hypertension. The plasma level of
aldosterone was increased, decreased, and remained unchanged in 2K1C,
DOCA/
salt, and
L-NAME hypertension, respectively. The down-regulation of 11β-HSD II may contribute to the
sodium retention, thereby increasing the blood pressure in 2K1C and
L-NAME hypertension. On the contrary, the up-regulation in
DOCA/
salt hypertension may play a compensatory role to dissipate the
sodium retention.