Schinke M, Baltatu O, Böhm M, Peters J, Rascher W, Bricca G, Lippoldt A, Ganten D, Bader M
Max-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Strasse 10, D-13092 Berlin-Buch, Germany.
Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3975-80. doi: 10.1073/pnas.96.7.3975.
Angiotensin produced systemically or locally in tissues such as the brain plays an important role in the regulation of blood pressure and in the development of hypertension. We have established transgenic rats [TGR(ASrAOGEN)] expressing an antisense RNA against angiotensinogen mRNA specifically in the brain. In these animals, the brain angiotensinogen level is reduced by more than 90% and the drinking response to intracerebroventricular renin infusions is decreased markedly compared with control rats. Blood pressure of transgenic rats is lowered by 8 mmHg (1 mmHg = 133 Pa) compared with control rats. Crossbreeding of TGR(ASrAOGEN) with a hypertensive transgenic rat strain exhibiting elevated angiotensin II levels in tissues results in a marked attenuation of the hypertensive phenotype. Moreover, TGR(ASrAOGEN) exhibit a diabetes insipidus-like syndrome producing an increased amount of urine with decreased osmolarity. The observed reduction in plasma vasopressin by 35% may mediate these phenotypes of TGR(ASrAOGEN). This new animal model presenting long-term and tissue-specific down-regulation of angiotensinogen corroborates the functional significance of local angiotensin production in the brain for the central regulation of blood pressure and for the pathogenesis of hypertension.
在诸如大脑等组织中全身或局部产生的血管紧张素在血压调节和高血压发展过程中发挥着重要作用。我们已经建立了在大脑中特异性表达针对血管紧张素原mRNA的反义RNA的转基因大鼠[TGR(ASrAOGEN)]。在这些动物中,与对照大鼠相比,大脑血管紧张素原水平降低了90%以上,对脑室内注射肾素的饮水反应明显降低。与对照大鼠相比,转基因大鼠的血压降低了8 mmHg(1 mmHg = 133 Pa)。将TGR(ASrAOGEN)与在组织中血管紧张素II水平升高的高血压转基因大鼠品系进行杂交,导致高血压表型明显减弱。此外,TGR(ASrAOGEN)表现出类似尿崩症的综合征,产生尿量增加且渗透压降低。观察到血浆血管加压素降低35%可能介导了TGR(ASrAOGEN)的这些表型。这种呈现血管紧张素原长期和组织特异性下调的新动物模型证实了大脑中局部血管紧张素产生对血压中枢调节和高血压发病机制的功能意义。