Renal c-fos expression induced by angiotensin II is enhanced in spontaneously hypertensive rats

被引:7
作者
Otsuka, F
Yamauchi, T
Ogura, T
Takabashi, M
Kageyama, J
Makino, H
机构
[1] Okayama Univ, Sch Med, Dept Med 3, Okayama 7008558, Japan
[2] Okayama Univ, Hlth & Med Ctr, Okayama 700, Japan
[3] Okayama Univ, Sch Hlth Sci, Dept Nursing, Okayama 700, Japan
关键词
angiotensin II; c-fos; in vivo c-fos expression; spontaneously hypertensive rats; kidney;
D O I
10.1016/S0024-3205(99)80005-8
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
We compared the effect of a bolus injection of angiotensin II (Ang TT) on the expression of protooncogene c-fos in the renal cortex and medulla of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Intravenous infusion of 5 ng/kg body weight of Ang II resulted in an immediate rise in systolic blood pressure (SBP) in both SHR and WKY rats. The percent rise in SEP was similar in both strains. Pretreatment with Ang II type 1 (AT1)-receptor antagonist, L-158,809 (1 mg/kg) abolished the presser response in both strains. Competitive reverse transcription-polymerase chain reaction (RT-PCR) showed that administration of Ang II increased the expression of c-fos mRNA within 10 min in both the renal cortex and medulla of SHR significantly higher than WKY rats. Moreover, the enhanced c-fos mRNA expression due to Ang II was significantly suppressed by the pretreatment of L158,809 in both strains. These findings indicate that c-fos expression in the kidney is mediated by AT1-receptors and that the renal c-fos response to exogenous Ang II was significantly augmented in SHR compared with WKY rats, suggesting that this hyperresponsiveness on renal AT1-action may partly contribute to the progression of renal injury in SHR.
引用
收藏
页码:2089 / 2095
页数:7
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