Marathias K P, Agroyannis B, Mavromoustakos T, Matsoukas J, Vlahakos D V
Onassis Cardiac Surgery Center, Athens, Greece.
Curr Top Med Chem. 2004;4(4):483-6. doi: 10.2174/1568026043451311.
Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary disease, and congestive heart failure. Accordingly, RAS inactivation may confer susceptibility to the hematocrit-lowering effects of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Indeed, a dose-dependent decrease in hematocrit is observed within the first month of such therapy. In the majority of patients with hypertension decreases in hematocrit values after RAS inactivation are small and not clinically important. In extreme conditions, however, such as erythrocytosis after successful renal transplantation, secondary polycythemia of chronically hypoxemic COPD patients, erythrocytosis associated with renovascular hypertension, severe cardiac or renal failure, the hematocrit-lowering effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blocker may be profound and even lead to or worsen anemia. Hematocrit reaches its nadir value within three months, and then it remains stable during long-term observations. After discontinuation of RAS blockade, hematocrit values rise gradually over the next three to four months towards the pretreatment levels. The mechanism(s) related to this phenomenon is not yet fully understood, but angiotensin II seems to be responsible for inappropriately sustaining secretion of erythropoietin despite hematocrit elevation and capable to directly stimulate the erythroid progenitors in bone marrow to produce erythrocytes.
多项临床和实验观察表明，完整且激活的肾素-血管紧张素系统（RAS）可能是多种临床病症（包括高血压、慢性肾功能不全或衰竭、慢性阻塞性肺疾病和充血性心力衰竭）中红细胞生成的重要决定因素。因此，RAS失活可能使人易受血管紧张素转换酶抑制剂或血管紧张素受体阻滞剂降低血细胞比容作用的影响。事实上，在这种治疗的第一个月内可观察到血细胞比容呈剂量依赖性下降。在大多数高血压患者中，RAS失活后血细胞比容值的下降幅度较小，且在临床上并不重要。然而，在极端情况下，如肾移植成功后的红细胞增多症、慢性低氧性慢性阻塞性肺疾病患者的继发性红细胞增多症、与肾血管性高血压相关的红细胞增多症、严重心脏或肾衰竭，血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂降低血细胞比容的作用可能很显著，甚至会导致贫血或使贫血加重。血细胞比容在三个月内降至最低点，然后在长期观察中保持稳定。停用RAS阻滞剂后，血细胞比容值在接下来的三到四个月内逐渐回升至治疗前水平。与这一现象相关的机制尚未完全明了，但血管紧张素II似乎在血细胞比容升高的情况下仍不适当地维持促红细胞生成素的分泌，并能够直接刺激骨髓中的红系祖细胞生成红细胞。
