Mantero F, Fallo F, Patrassi G, Sarandria A, Pedini F, Girolami A
Clin Exp Hypertens A. 1982;4(11-12):2425-34. doi: 10.3109/10641968209062400.
It has been suggested that a Factor XII-plasma Prekallikrein dependent pathway might play an important role in the activation of inactive renin. Since Captopril has the potential to affect the kinin-kallikrein system, we have studied in a group of 16 patients with essential hypertension its acute effect both on the levels of active, inactive and total renin, and on the contact phase of the coagulation system. Our results show that a single dose of Captopril (25 mg) induces a rapid and persistent increase of active and total renin, while inactive renin tends to decrease. Together with blood pressure, plasma Prekallikrein(PK), Factor XII(FXII) and Factor XI(FXI) concomitantly decrease, although not significantly, and their values seem to return to basal levels soonafter. However, no correlation was found at any time between the levels of any of these coagulation factors, including PK, and those of inactive, active or the ratio inactive/total renin. In spite of that, it is still possible that an activation of PK, which is likely to occur under Captopril administration, may affect at least the conversion of vessel-bound prorenin rather than the circulating form.
有人提出,依赖于因子 XII - 血浆前激肽释放酶的途径可能在无活性肾素的激活中起重要作用。由于卡托普利有可能影响激肽 - 激肽释放酶系统,我们对一组 16 例原发性高血压患者进行了研究,观察其对活性肾素、无活性肾素和总肾素水平以及凝血系统接触相的急性影响。我们的结果表明,单剂量卡托普利(25 毫克)可导致活性肾素和总肾素迅速且持续升高,而无活性肾素则趋于降低。与血压一起,血浆前激肽释放酶(PK)、因子 XII(FXII)和因子 XI(FXI)虽无显著下降,但也随之降低,且其值似乎在不久后就恢复到基础水平。然而,在任何时候,这些凝血因子(包括 PK)的水平与无活性肾素、活性肾素或无活性肾素/总肾素比值之间均未发现相关性。尽管如此,在卡托普利给药过程中可能发生的 PK 激活仍有可能至少影响血管结合型肾素原的转化,而非循环形式的肾素原。