Faensen Anne Lena, von Trebra Markus Wehland, Freese Florian, Kreutz Reinhold, Bamberg Christian, Hinkson Larry, Rothermund Lars
J Perinat Med. 2016 Aug 1;44(6):705-9. doi: 10.1515/jpm-2015-0159.
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.
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).
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).
Altered fetal expression of key molecules of the renin-angiotensin system in MWF indicates a possible role in genetic low nephron number hypertension.
本研究调查肾素 - 血管紧张素系统（RAS）的关键组成部分，其在肾发生中起核心作用，并且可能在成年期动脉高血压的胎儿编程中发挥作用。
我们将一种具有先天性肾单位缺陷的遗传大鼠模型，即慕尼黑Wistar Fromter大鼠（MWF），与正常血压的Wistar大鼠在胎儿发育第19天（E19）和出生后第7天（D7）的肾发生过程中进行比较。
在E19时，与Wistar大鼠（n = 8）相比，MWF（n = 8）中血管紧张素II 1a型（AT1a）受体（-50%，P<0.05）和1b型（AT1b）受体（-55%，P<0.05）的肾mRNA显著降低，血管紧张素II 2型（AT2）受体的肾mRNA表达增加了五倍。在D7时，与Wistar大鼠（n = 7）相比，MWF（n = 8）中AT1a的肾mRNA表达（-42%，P<0.05）仍然较低。MWF（n = 8）中AT2的肾mRNA表达（-30%，P>0.05）下降至约Wistar对照（n = 6）的水平。
MWF中肾素 - 血管紧张素系统关键分子的胎儿表达改变表明其在遗传性低肾单位数高血压中可能发挥作用。
