Peters J, Ganten D
Pharmakologisches Institut, Universität Heidelberg, Germany.
Horm Metab Res. 1998 Jun-Jul;30(6-7):350-4. doi: 10.1055/s-2007-978897.
Transgenic rats, termed TGR(mREN2)27, have been generated carrying the mouse ren-2 renin gene. As intended the gene was expressed highly within the adrenal gland offering the opportunity to study the intraadrenal renin-angiotensin system in vivo. Concomitantly with increased adrenal renin activity, the production of adrenocortical steroids are elevated and the regulation of aldosterone production is impaired in TGR(mREN2)27. Furthermore, the transgenic rats develop severe sodium dependent hypertension. Since kidney and plasma renin concentrations and plasma angiotensins are low in the transgenic model, those factors cannot account for the altered regulation of aldosterone production. Instead the experiments with TGR(mREN2)27 demonstrate the functional role of the local adrenal renin-angiotensin system.
转基因大鼠,称为TGR(mREN2)27,已被培育出携带小鼠肾素-2肾素基因。正如预期的那样,该基因在肾上腺内高度表达,为体内研究肾上腺内肾素-血管紧张素系统提供了机会。与肾上腺肾素活性增加同时,TGR(mREN2)27中肾上腺皮质类固醇的产生增加,醛固酮产生的调节受损。此外,转基因大鼠发展为严重的钠依赖性高血压。由于在转基因模型中肾脏和血浆肾素浓度以及血浆血管紧张素较低,这些因素不能解释醛固酮产生调节的改变。相反,对TGR(mREN2)27的实验证明了局部肾上腺肾素-血管紧张素系统的功能作用。