Sugio K, Greenbaum L M
Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912.
Inflammation. 1988 Oct;12(5):407-12. doi: 10.1007/BF00919434.
The vascular permeability-increasing response to T-kinin in rat and guinea pig skin was investigated. The vascular permeability was measured with 125I-labeled bovine serum albumin [( 125I]BSA) as a tracer. Plasma exudation rapidly occurred 0-15 min after the intradermal injection of T-kinin. T-kinin in doses of 0.3, 1, and 3 nM/spot significantly increased the vascular permeability in a dose-dependent manner. The vascular response of T-kinin is similar to that of bradykinin. On the other hand, T-kinin analogs, D-Ile-Ser-bradykinin and Ile-D-Ser-bradykinin only weakly enhanced the vascular permeability. Prostaglandin E1, forskolin, and the angiotensin-converting enzyme inhibitor, SQ-14225, potentiated the T-kinin-induced plasma exudation. Cyproheptadine and indomethacin did not affect the T-kinin-induced response. The results suggest that T-kinin will play an important role in increasing vascular permeability associated with inflammation.
研究了大鼠和豚鼠皮肤对T-激肽的血管通透性增加反应。以125I标记的牛血清白蛋白([125I]BSA)作为示踪剂测量血管通透性。皮内注射T-激肽后0-15分钟迅速发生血浆渗出。剂量为0.3、1和3 nM/点的T-激肽以剂量依赖性方式显著增加血管通透性。T-激肽的血管反应与缓激肽相似。另一方面,T-激肽类似物D-异亮氨酸-丝氨酸-缓激肽和异亮氨酸-D-丝氨酸-缓激肽仅微弱增强血管通透性。前列腺素E1、福斯可林和血管紧张素转换酶抑制剂SQ-14225增强了T-激肽诱导的血浆渗出。赛庚啶和吲哚美辛不影响T-激肽诱导的反应。结果表明,T-激肽在增加与炎症相关的血管通透性方面将发挥重要作用。