Riabov S I, Kucher A G, Kotovoĭ Iu O, Kaiukov I G
Klin Med (Mosk). 1990 Dec;68(12):22-5.
A total of 74 patients with various clinicomorphological variants of glomerulonephritis (GN) were examined. Only a high activity of the enzyme kinase-1 that destroys kinins and the kallikrein inhibitors alpha 1-antitrypsin, alpha 2-macroglobulin is a contribution of the kallikrein-kinin system made to the general antihypertensive "armoury" of the body, as shown by the study. The correlation between the kallikrein activity and the active renin/total renin ratio predetermines that kallikrein may participate in endogenous plasma renin activation in GN patients. In this case, the vasoconstrictive effect of renin may limit the antihypertensive action of kallikrein and kinins by a feedback mechanism.
共检查了74例患有各种临床形态学类型肾小球肾炎（GN）的患者。研究表明，只有破坏激肽和激肽释放酶抑制剂α1-抗胰蛋白酶、α2-巨球蛋白的酶激酶-1的高活性，才是激肽释放酶-激肽系统对机体总体降压“武器库”的贡献。激肽释放酶活性与活性肾素/总肾素比值之间的相关性预先确定了激肽释放酶可能参与GN患者内源性血浆肾素的激活。在这种情况下，肾素的血管收缩作用可能通过反馈机制限制激肽释放酶和激肽的降压作用。
