Cline M J, Melmon K L
Science. 1966 Sep 2;153(3740):1135-8. doi: 10.1126/science.153.3740.1135.
Kinins are naturally occurring vasoactive polypeptides thought to be mediators of acute inflammatory responses. Kinins are released from a plasma protein substrate by glass-activated plasma enzymes (kallikreins) or by isolated intact granulocytes. Cortisol in concentrations of 2.5 x 10(-6) to 2.5 x 10(-5)M prevented the release of active kinin from substrate by granulocytes or contact with glass. Deoxycorticosterone, progesterone, and etiocholanolone in comparable concentrations were significantly less effective in preventing kinin release. Plasma obtained from patients receiving prednisone released no kinin after activation by glass and less kinin than control plasma when exposed to granulocytes. Cortisol also partially inhibited the release of kinin by purified urinary kallikrein. Certain adrenocorticosteroids may exert their anti-inflammatory effect by inhibiting the release of plasma kinins. Steroids may act in part by preventing interaction between the activated kallikrein and its substrate.
激肽是天然存在的血管活性多肽,被认为是急性炎症反应的介质。激肽由玻璃激活的血浆酶(激肽释放酶)或分离的完整粒细胞从血浆蛋白底物中释放出来。浓度为2.5×10⁻⁶至2.5×10⁻⁵M的皮质醇可阻止粒细胞从底物中释放活性激肽或阻止其与玻璃接触。浓度相当的脱氧皮质酮、孕酮和表雄酮在阻止激肽释放方面的效果明显较差。接受泼尼松治疗的患者的血浆在经玻璃激活后不释放激肽,且在暴露于粒细胞时释放的激肽比对照血浆少。皮质醇还部分抑制纯化的尿激肽释放酶释放激肽。某些肾上腺皮质类固醇可能通过抑制血浆激肽的释放发挥其抗炎作用。类固醇可能部分通过阻止活化的激肽释放酶与其底物之间的相互作用而起作用。