Altered Regulation of 11beta-hydroxysteroid Dehydrogenase II in the Kidney of Rats with Experimental Hypertension.
- Author:
Seong Su KANG
1
;
Soo Wan KIM
;
Jong Un LEE
Author Information
- Publication Type:Original Article
- Keywords: Type II 11beta-hydroxysteroid dehydrogenase; Kidney; Hypertension
- MeSH: 11-beta-Hydroxysteroid Dehydrogenases*; Aldosterone; Animals; Blood Pressure; Blotting, Northern; Desoxycorticosterone; Down-Regulation; Humans; Hypertension*; Kidney*; Male; NG-Nitroarginine Methyl Ester; Plasma; Radioimmunoassay; Rats*; RNA, Messenger; Sodium; Up-Regulation
- From:Electrolytes & Blood Pressure 2007;5(2):89-94
- CountryRepublic of Korea
- Language:English
- Abstract: The present study was aimed at investigating the role of type II 11beta-hydroxysteroid dehydrogenase (IIbeta- HSD II) in the development of hypertension. Two-kidney, one-clip (2K1C), deoxycorticosterone acetate (DOCA)/salt, or NG-nitro-L-arginine methyl ester (L-NAME) hypertension was induced in male Sprague- Dawley rats. Four weeks later, the expression of 11beta-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 11beta-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 11beta-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.
