Article
Effect of gender and estradiol on the expression Ang II type-2 (AT2) receptors in the rat kidney
Einfluss von Geschlecht und Estradiol auf die Expression von Ang II Typ-2 (AT2) Rezeptoren in der Ratten-Niere
Search Medline for
Authors
Published: | November 11, 2004 |
---|
Outline
Text
Background
Sex differences in renal hemodynamics and in the occurrence and progression of renal disease are well recognized. This gender dependency is also apparent in the renal response to Ang II. However, although AT1 receptors have been shown to be regulated by estrogens in various tissues, the effect of gender and estrogens on renal Ang II receptor expression has not been clarified. Therefore, we analyzed possible gender-related differences in the gene expression of renal angiotensin (Ang II) receptors and of Ang II converting enzyme (ACE) and their regulation by estrogens in female rats.
Methods
The mRNA levels of AT1A, AT1B and AT2 receptors and ACE were measured in the kidneys of male and female rats by quantitative real-time RT-PCR. In addition, female rats were either sham-operated or ovariectomized and subsequently treated with placebo or 17beta-estradiol for 21 days and the effect of estradiol on the renal mRNA expression of Ang II receptor subtypes and ACE were analyzed.
Results
In female rats, the mRNA levels of renal AT2 receptors were significantly elevated while the mRNA levels of ACE were significantly reduced compared to male rats. No differences were observed in the mRNA levels of renal AT1A and AT1B receptors between male and female rats. Ovariectomy significantly decreased the mRNA levels of renal AT2 receptors compared to sham-operated rats. In contrast, renal ACE mRNA was increased after ovariectomy. Treatment with 17beta-estradiol reversed the effects of ovariectomy on the AT2 receptor and ACE mRNA.
Conclusions
Besides the gender differences in renal ACE, renal AT2 receptors are increased in female rats and endogenous estradiol appears responsible for these differences. The known gender differences of the renal response to Ang II may partially depend on the differential expression of renal AT2 receptors.