Prescott G, Silversides D W, Chiu S M, Reudelhuber T L
Laboratory of Molecular Biochemistry of Hypertension, Clinical Research Institute of Montreal, Montreal, Quebec H2W 1R7, Canada.
Physiol Genomics. 2000 Nov 9;4(1):67-73. doi: 10.1152/physiolgenomics.2000.4.1.67.
The activity of a local cardiac renin-angiotensin system (RAS) has long been suspected in the promotion of cardiac pathologies including hypertrophy, ischemia, and infarction. All of the components of the RAS cascade have been demonstrated to be synthesized within the heart with the possible exception of the first enzyme in the cascade, renin. In the current study, we provide direct evidence that circulating renin can contribute to cardiac-specific synthesis of angiotensin peptides. Furthermore, we demonstrate this effect is independent of blood pressure and that in animals of comparable blood pressure, elevated circulating renin significantly enhances cardiac fibrosis. These results may serve to explain some of the cardiac pathologies associated with the RAS.
长期以来，人们一直怀疑局部心脏肾素-血管紧张素系统（RAS）的活性在促进包括肥大、缺血和梗死在内的心脏病理过程中发挥作用。肾素-血管紧张素系统级联反应的所有成分已被证明可在心脏内合成，级联反应中的第一种酶肾素可能是个例外。在本研究中，我们提供了直接证据，表明循环肾素可促进心脏特异性血管紧张素肽的合成。此外，我们证明这种作用与血压无关，在血压相当的动物中，循环肾素升高会显著增强心脏纤维化。这些结果可能有助于解释一些与肾素-血管紧张素系统相关的心脏病理情况。
