Imamura T, Yamamoto T, Kambara T
Am J Pathol. 1984 Apr;115(1):92-101.
Plasma kallikrein (mol wt 80,000) was purified from guinea pig plasma, and it caused vascular permeability enhancement when injected into guinea pig skin. The activity had a linear relationship to the logarithm of kallikrein concentrations from 5 X 10(-9) M to 5 X 10(-6) M and was blocked by immunopurified anti-prekallikrein F(ab')2 rabbit antibody and soybean trypsin inhibitor. Carboxypeptidase B(1.7 units), a kinin-destructive enzyme, decreased the permeability activity to 1/20, while SQ 20,881 (10(-6) M), an inhibitor to a kinin-destructive enzyme, augmented the activity 5.4-fold. These results suggested that the permeability activity of kallikrein was performed finally through kinin generation in the skin. The permeability activity was short-lasting, and was completely blocked by a kallikrein inhibitor purified from guinea pig plasma, suggesting the presence of a down-regulation system for the permeability activity in vivo. Prostaglandin E2 (25 ng), a hyperemia inducer in microcirculation, augmented the permeability activity 12-fold, suggesting the presence of an up-regulation system in vivo. Accordingly, it was assumed that kallikrein-kinin system might play a role as a vascular permeability enhancement system in guinea pig skin.
从豚鼠血浆中纯化出分子量为80,000的血浆激肽释放酶，将其注入豚鼠皮肤时可引起血管通透性增强。该活性与激肽释放酶浓度在5×10⁻⁹M至5×10⁻⁶M范围内的对数呈线性关系，并被免疫纯化的抗前激肽释放酶F(ab')₂兔抗体和大豆胰蛋白酶抑制剂所阻断。羧肽酶B（1.7单位）是一种激肽破坏酶，可使通透性活性降低至1/20，而激肽破坏酶抑制剂SQ 20,881（10⁻⁶M）可使活性增强5.4倍。这些结果表明，激肽释放酶的通透性活性最终是通过皮肤中激肽的生成来实现的。该通透性活性持续时间较短，并被从豚鼠血浆中纯化的激肽释放酶抑制剂完全阻断，提示体内存在针对该通透性活性的下调系统。前列腺素E₂（25 ng）是微循环中的充血诱导剂，可使通透性活性增强12倍，提示体内存在上调系统。因此，推测激肽释放酶-激肽系统可能在豚鼠皮肤中作为血管通透性增强系统发挥作用。
