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Licensed Unlicensed Requires Authentication Published by De Gruyter December 17, 2015

Genetic low nephron number hypertension is associated with altered expression of key components of the renin-angiotensin system during nephrogenesis

  • Anne Lena Faensen EMAIL logo , Markus Wehland von Trebra , Florian Freese , Reinhold Kreutz , Christian Bamberg , Larry Hinkson and Lars Rothermund

Abstract

Aim:

This study investigates key components of the renin-angiotensin system (RAS) which play a central role in nephrogenesis and possibly in fetal programming of arterial hypertension in adult life.

Methods:

We compared a genetic rat model with inborn nephron deficit, the Munich Wistar Fromter rat (MWF), to normotensive Wistar rats during nephrogenesis at day 19 of fetal development (E19) and at postnatal day 7 (D7).

Results:

At E19 renal mRNA of angiotensin II type 1a (AT1a) (–50%, P<0.05) and type 1b (AT1b) (–55%, P<0.05) receptors were significantly decreased and renal mRNA expression of angiotensin II type 2(AT2)receptor was fivefold increased in MWF (n=8) as compared to Wistar rats (n=8). At D7 renal mRNA expression of AT1a (–42%, P<0.05) remained lower in MWF (n=8) as compared to Wistar (n=7). Renal mRNA expression of AT2 (–30%, P>0.05) decreased in MWF (n=8) to about the level of the Wistar control (n=6).

Conclusions:

Altered fetal expression of key molecules of the renin-angiotensin system in MWF indicates a possible role in genetic low nephron number hypertension.


Corresponding author: Anne Lena Faensen, née Freese, Klinik für Geburtsmedizin, Charité-Universitätsmedizin, Augustenburgerplatz 1, 13353 Berlin, Germany, Tel.: +49-30-450564072, Fax: +49-30-450564901, E-mail: ; und Institut für Klinische Pharmakologie und Toxikologie, Charité-Universitätsmedizin Berlin, Berlin, Germany

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The authors stated that there are no conflicts of interest regarding the publication of this article.



Article note:

Supported by the Deutsche Forschungsgemeinschaft (DFG,GrantRO 2124/2-1 and RO 2124/2-2).


Received: 2015-6-2
Accepted: 2015-11-2
Published Online: 2015-12-17
Published in Print: 2016-8-1

©2016 Walter de Gruyter GmbH, Berlin/Boston

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