The possible roles of mineralocorticoid receptor and 11β-hydroxy steroid dehydrogenase type 2 in cardiac fibrosis in the spontaneously hypertensive rat

被引:33
作者
Konishi, A
Tazawa, C
Miki, Y
Darnel, AD
Suzuki, T
Ohta, Y
Suzuki, T
Tabayashi, K
Sasano, H
机构
[1] Tohoku Univ, Grad Sch Med, Dept Pathol, Aoba Ku, Sendai, Miyagi 9808575, Japan
[2] Tohoku Univ, Grad Sch Med, Dept Cardiovasc Surg, Sendai, Miyagi 9808575, Japan
[3] Kinki Univ, Sch Med, Dept Pathol 1, Sayama, Osaka 5898511, Japan
关键词
SHR; hypertension; cardiac fibrosis; mineralocorticoid receptor; 11 beta-hydroxysteroid dehydrogenase type 2;
D O I
10.1016/S0960-0760(03)00198-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In hypertension, aldosterone has been demonstrated to play a crucial role in cardiac fibrosis, which generally increases cardiac morbidity and death. However, few studies have reported the expression of the mineralocorticoid receptor (MR) and 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in the heart under hypertensive conditions. Therefore, in this study, spontaneously hypertensive rats (SHR) were examined to elucidate the possible actions of mineralocorticoids via binding to MR. Wister Kyoto Rat (WKY), SHR, stroke-prone SHR (SHRSP), and malignant SHRSP (M-SHRSP) were used. Total RNA was extracted from the left ventricle of these rats, and examined for the expression levels of MR, 11beta-HSD2 and Collagen types 1 and 3 using reverse transcription real-time quantitative polymerase chain reaction employing the Light Cycler Instrument. Blood pressure was significantly different among each group. The mean mRNA levels for MR, 11beta-HSD2 and Collagen types 1 and 3 in M-SHRSP were found to be significantly increased compared to those of WKY, whereas no significant differences in mRNA levels were detected among SHR and SHRSP. Findings from the present study appear to demonstrate that MR and 11beta-HSD2 mRNA significantly rise in the left ventricle of M-SHRSP and increase of these mRNA is one of the cause of cardiac fibrosis. (C) 2003 Elsevier Ltd. All rights reserved.
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页码:439 / 442
页数:4
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