Abstract
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.