Llorens-Cortes C, Greenberg B, Huang H, Corvol P
INSERM U36, Collège de France, Paris.
Hypertension. 1994 Nov;24(5):538-48. doi: 10.1161/01.hyp.24.5.538.
Recent studies have revealed that angiotensin II (Ang II) interacts with two pharmacologically different types of seven-transmembrane domain receptors, hence named Ang II type 1 and type 2 (AT1 and AT2) receptors. cDNAs for the AT1 receptor have been cloned, and the existence of two receptor subtypes, AT1A and AT1B, has been revealed in rat and mouse. This study presents a new approach for the specific quantification of AT1A and AT1B receptor mRNAs by reverse transcription and polymerase chain reaction amplification in the presence of an AT1 receptor mutant cRNA as internal standard. Absolute quantities of mRNA are then determined by extrapolation using the standard curve generated with the internal standard. Moreover, addition of this internal standard to each tube controls for both reverse transcription and polymerase chain reaction amplification in each sample. In male Wistar rats, the highest absolute AT1A receptor mRNA levels were found in liver and kidney and those for AT1B receptor mRNA in the pituitary. Expressed as a percentage of total AT1A+AT1B receptor mRNA content, AT1A receptor mRNA content was 100% in liver, 85% in lung, 73% in kidney, 65% in aorta, 48% in adrenals, and 15% in the hypophysis. Since this approach can determine absolute AT1A and AT1B receptor mRNA quantities in different organs, it allows the study of the regulation of their expression under different pathophysiological conditions. After sodium depletion, known to induce hyperactivity of the renin-angiotensin system, adrenal AT1A and AT1B receptor mRNA levels were increased by 60% and 110%, respectively. In contrast, in renovascular hypertension (two-kidney, one clip), also associated with elevated circulating plasma renin activity, adrenal AT1B receptor mRNA levels decreased by 50%, whereas there was no change in those of AT1A. Therefore, the differential distribution and regulation of these two receptor subtypes suggest that each of them might be involved in the mediation of different biological effects of Ang II.
最近的研究表明,血管紧张素II(Ang II)与两种药理学特性不同的七跨膜结构域受体相互作用,因此分别命名为血管紧张素II 1型和2型(AT1和AT2)受体。AT1受体的cDNA已被克隆,并且在大鼠和小鼠中发现了两种受体亚型,即AT1A和AT1B。本研究提出了一种新方法,即在存在AT1受体突变体cRNA作为内标的情况下,通过逆转录和聚合酶链反应扩增对AT1A和AT1B受体mRNA进行特异性定量。然后使用由内标生成的标准曲线通过外推法确定mRNA的绝对量。此外,向每个管中添加该内标可控制每个样品中的逆转录和聚合酶链反应扩增。在雄性Wistar大鼠中,肝脏和肾脏中AT1A受体mRNA的绝对水平最高,垂体中AT1B受体mRNA的绝对水平最高。以AT1A + AT1B受体mRNA总含量的百分比表示,肝脏中AT1A受体mRNA含量为100%,肺中为85%,肾脏中为73%,主动脉中为65%,肾上腺中为48%,垂体中为15%。由于这种方法可以确定不同器官中AT1A和AT1B受体mRNA的绝对量,因此可以研究它们在不同病理生理条件下的表达调控。已知钠耗竭会诱导肾素-血管紧张素系统的活性增强,肾上腺中AT1A和AT1B受体mRNA水平分别增加了60%和110%。相反,在肾血管性高血压(两肾一夹)中,循环血浆肾素活性也升高,肾上腺中AT1B受体mRNA水平下降了50%,而AT1A受体mRNA水平没有变化。因此,这两种受体亚型的差异分布和调控表明它们各自可能参与了Ang II不同生物学效应的介导。